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Overall cheap erectile dysfunction pills online uk buy generic levitra oral jelly 20mg line, considerably more current flows downward from the base of the ventricles toward the apex than in the upward direction. Therefore, the summated vector of the generated potential at this particular instant, called the instantaneous mean vector, is represented by the long black arrow drawn through the center of the ventricles in a direction from the base toward the apex. Furthermore, because the summated current is quite large, the potential is large, and the vector is long. In this case, the direction of the vector is +55 degrees, and the voltage of the potential, represented by the length of vector A, is 2 millivolts. In the diagram below the heart, vector A is shown again, and a line is drawn to represent the axis of lead I in the 0-degree direction. To determine how much of the voltage in vector A will be recorded in lead I, a line perpendicular to the axis of lead I is drawn from the tip of vector A to the lead I axis, and a so-called projected vector (B) is drawn along the lead I axis. The instantaneous recorded voltage will be equal to the length of B divided by the length of A times 2 millivolts, or about 1 millivolt. In this example, vector A represents the electrical potential and its axis at a given instant during ventricular depolarization in a heart in which the left side of the heart depolarizes more rapidly than the right side. In this case, the instantaneous vector has a direction of 100 degrees, and its voltage is again 2 millivolts. To determine the potential actually recorded in lead I, we draw a perpendicular line from the tip of vector A to the lead I axis and find projected vector B. Each of these vectors is then analyzed by the method described in the preceding section to determine the voltages that will be recorded at each instant in each of the three standard electrocardiographic leads. At this time, the vector is short because only a small portion of the ventricles-the septum-is depolarized. Therefore, all electrocardiographic voltages are low, as recorded to the right of the ventricular muscle for each of the leads. Also, the axis of the vector is beginning to shift toward the left side of the chest because the left ventricle is slightly slower to depolarize than the right ventricle. When it occurs, it is caused by initial depolarization of the left side of the septum before the right side, which creates a weak vector from left to right for a fraction of a second before the usual base to apex vector occurs. Because the septum and endocardial areas of the ventricular muscle depolarize first, it seems logical that these areas should repolarize first as well. However, this is not the usual case, because the septum and other endocardial areas have a longer period of contraction than most of the external surfaces of the heart. Therefore, the greatest portion of ventricular muscle mass to repolarize first is the entire outer surface of the ventricles, especially near the apex of the heart. This sequence of repolarization is postulated to be caused by the high blood pressure inside the ventricles during contraction, which greatly reduces coronary blood flow to the endocardium, thereby slowing repolarization in the endocardial areas. Because the outer apical surfaces of the ventricles repolarize before the inner surfaces, the positive end of the overall ventricular vector during repolarization is toward the apex of the heart. At each stage, the vector extends from the base of the heart toward the apex until it disappears in the last stage. At first, the vector is relatively small because the area of repolarization is small. Finally, the vector becomes weaker again because the areas of depolarization still persisting become so slight that the total quantity of current flow decreases. These changes also demonstrate that the vector is greatest when about half the heart is in the polarized state and about half is depolarized. Furthermore, the vector remains generally in this direction throughout the process of normal atrial depolarization. Spread of depolarization through the atrial muscle is much slower than in the ventricles because the atria have no Purkinje system for fast conduction of the depolarization signal. Therefore, the musculature around the sinus node becomes depolarized a long time before the musculature in distal parts of the atria. Consequently, the area in the atria that also becomes repolarized first is the sinus nodal region, the area that had originally become depolarized first. Therefore, the atrial repolarization vector is backward to the vector of depolarization. Vectorcardiogram As noted previously, the vector of current flow through the heart changes rapidly as the impulse spreads through the myocardium. First, the vector increases and decreases in length because of increasing and decreasing voltage of the vector. Second, the vector changes direction because of changes in the average direction of the electrical potential from the heart. While the heart muscle is polarized between heartbeats, the positive end of the vector remains at the zero point because there is no vectorial electrical potential. However, as soon as current begins to flow through the ventricles at the beginning of ventricular depolarization, the positive end of the vector leaves the zero reference point. When the septum first becomes depolarized, the vector extends downward toward the apex of the ventricles, but it is relatively weak, thus generating the first portion of the ventricular vectorcardiogram, as shown by the positive end of vector 1. As more of the ventricular muscle becomes depolarized, the vector becomes stronger and stronger, usually swinging slightly to one side. Finally, the ventricles become totally depolarized, and the vector becomes zero once again, as shown at point 5. This preponderant direction of the potential during depolarization from the base to the apex of the heart is called the mean electrical axis of the ventricles. In many pathological conditions of the heart, this direction changes markedly, sometimes even to opposite poles of the heart. The causes of the normal variations are mainly anatomical differences in the Purkinje distribution system or in the musculature itself of different hearts. However, a number of abnormal conditions of the heart can cause axis deviation beyond the normal limits, as described below. Consequently, the normal ventricle becomes depolarized considerably in advance of the hypertrophied ventricle, and this situation causes a strong vector from the normal side of the heart toward the hypertrophied side, which remains strongly positively charged.

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Frequency distribution curves of the arterial pressure for a 24-hour period in a normal dog and in the same dog several weeks after the baroreceptors had been denervated erectile dysfunction family doctor order levitra oral jelly 20mg line. Two-hour records of arterial pressure in a normal dog (top) and in the same dog (bottom) several weeks after the baroreceptors had been denervated. Because the baroreceptor system opposes in- creases or decreases in arterial pressure, it is called a pressure buffer system, and the nerves from the baroreceptors are called buffer nerves. The upper panel in this figure shows an arterial pressure recording for 2 hours from a normal dog, and the lower panel shows an arterial pressure recording from a dog whose baroreceptor nerves from the carotid sinuses and the aorta had been removed. Note the extreme variability of pressure in the denervated dog caused by simple events of the day, such as lying down, standing, excitement, eating, defecation, and noises. Note that when the baroreceptors were functioning normally, the mean arterial pressure remained within a narrow range of between 85 and 115 mm Hg throughout the day and, for most of the day, it remained at about 100 mm Hg. After denervation of the baroreceptors, however, the frequency distribution curve flattened, showing that the pressure range increased 2. Thus, one can see the extreme variability of pressure in the absence of the arterial baroreceptor system. One reason that the baroreceptors have been considered by some physiologists to be relatively unimportant in chronic regulation of arterial pressure is that they tend to reset in 1 to 2 days to the pressure level to which they are exposed. That is, if the arterial pressure rises from the normal value of 100 to 160 mm Hg, a very high rate of baroreceptor impulses is at first transmitted. Then, it diminishes much more slowly during the next 1 to 2 days, at the end of which time the rate of firing will have returned to nearly normal, despite the fact that the mean arterial pressure still remains at 160 mm Hg. Conversely, when the arterial pressure falls to a very low level, the baroreceptors at first transmit no impulses but gradually, over 1 to 2 days, the rate of baroreceptor firing returns toward the control level. This resetting of the baroreceptors may attenuate their potency as a control system for correcting disturbances that tend to change arterial pressure for longer than a few days at a time. Experimental studies, however, have suggested that the baroreceptors do not completely reset and may therefore contribute to long-term blood pressure regulation, especially by influencing sympathetic nerve activity of the kidneys. This action, in turn, causes a gradual decrease in blood volume, which helps restore arterial pressure toward normal. Experimental studies and clinical trials have shown that chronic electrical stimulation of carotid sinus afferent nerve fibers can cause sustained reductions in sympathetic nervous system activity and arterial pressure of at least 15 to 20 mm Hg. These observations suggest that most, if not all, the baroreceptor reflex resetting that occurs when increases in arterial pressure are sustained, as in chronic hypertension, is due to resetting of the carotid sinus nerve mechanoreceptors themselves rather than resetting in central nervous system vasomotor centers. Control of Arterial Pressure by the Carotid and Aortic Chemoreceptors-Effect of Low Oxygen on Arterial Pressure. Closely associated with the baroreceptor pres- in conditions such as severe obesity and obstructive sleep apnea, a serious sleep disorder associated with repetitive episodes of nocturnal breathing cessation and hypoxia. The atria and pulmonary arteries have stretch sure control system is a chemoreceptor reflex that operates in much the same way as the baroreceptor reflex except that chemoreceptors, instead of stretch receptors, initiate the response. The chemoreceptor cells are sensitive to low oxygen or elevated carbon dioxide and hydrogen ion levels. They are located in several small chemoreceptor organs about 2 millimeters in size (two carotid bodies, one of which lies in the bifurcation of each common carotid artery, and usually one to three aortic bodies adjacent to the aorta). Each carotid or aortic body is supplied with an abundant blood flow through a small nutrient artery, so the chemoreceptors are always in close contact with arterial blood. Whenever the arterial pressure falls below a critical level, the chemoreceptors become stimulated because diminished blood flow causes decreased oxygen, as well as excess buildup of carbon dioxide and hydrogen ions that are not removed by the slowly flowing blood. The signals transmitted from the chemoreceptors excite the vasomotor center, and this response elevates the arterial pressure back toward normal. However, this chemoreceptor reflex is not a powerful arterial pressure controller until the arterial pressure falls below 80 mm Hg. Therefore, it is at the lower pressures that this reflex becomes important to help prevent further decreases in arterial pressure. The chemoreceptors are discussed in much more detail in Chapter 42 in relation to respiratory control, in which they normally play a far more important role than in blood pressure control. However, activation of the chemoreceptors may also contribute to increases in arterial pressure 224 receptors in their walls called low-pressure receptors. Lowpressure receptors are similar to the baroreceptor stretch receptors of the large systemic arteries. These low-pressure receptors play an important role, especially in minimizing arterial pressure changes in response to changes in blood volume. For example, if 300 milliliters of blood suddenly are infused into a dog with all receptors intact, the arterial pressure rises only about 15 mm Hg. If the low-pressure receptors also are denervated, the arterial pressure rises about 100 mm Hg. Thus, one can see that even though the low-pressure receptors in the pulmonary artery and in the atria cannot detect the systemic arterial pressure, they do detect simultaneous increases in pressure in the low-pressure areas of the circulation caused by increase in volume. Also, they elicit reflexes parallel to the baroreceptor reflexes to make the total reflex system more potent for control of arterial pressure. The decreased afferent arteriolar resistance in the kidneys causes the glomerular capillary pressure to rise, with a resultant increase in filtration of fluid into the kidney tubules. The combination of these effects-an increase in glomerular filtration and a decrease in reabsorption of the fluid-increases fluid loss by the kidneys and attenuates the increased blood volume. All these mechanisms that tend to return blood volume back toward normal after a volume overload act indirectly as pressure controllers, as well as blood volume controllers, because excess volume drives the heart to greater cardiac output and higher arterial pressure. This volume reflex mechanism is discussed again in Chapter 30, along with other mechanisms of blood volume control. Reflex responses to increased blood volume which increase arterial pressure and atrial stretch.

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This figure demonstrates that a 3 protein shake erectile dysfunction 20 mg levitra oral jelly purchase visa,000 cycles/sec sound can be heard even when its intensity is as low as 70 decibels below 1 dyne/cm2 sound pressure level, which is one ten-millionth microwatt per square centimeter. Conversely, a 100 cycles/sec sound can be detected only if its intensity is 10,000 times as great as this. The frequencies of sound that a young person can hear are between 20 and 20,000 cycles/sec. Single nerve fibers entering the cochlear nuclei Primary auditory cortex Midbrain Medial geniculate nucleus (thalamus) Midbrain Inferior colliculus from the auditory nerve can fire at rates up to at least 1000/ sec, with the rate being determined mainly by the loudness of the sound. At sound frequencies up to 2000 to 4000 cycles/sec, the auditory nerve impulses are often synchronized with the sound waves, but they do not necessarily occur with every wave. In the auditory tracts of the brain stem, the firing is usually no longer synchronized with the sound frequency, except at sound frequencies below 200 cycles/sec. Above the level of the inferior colliculi, even this synchronization is mainly lost. These findings demonstrate that the sound signals are not transmitted unchanged directly from the ear to the higher levels of the brain; instead, information from the sound signals begins to be dissected from the impulse traffic at levels as low as the cochlear nuclei. We will have more to say about this subject later, especially in relation to perception of direction from which sound comes. The primary auditory cortex is directly excited by projections from the medial geniculate body, whereas the auditory association areas are excited secondarily by impulses from the primary auditory cortex, as well as by some projections from thalamic association areas adjacent to the medial geniculate body. At least six tonotopic maps have been Pons Nucleus of the lateral lemniscus Pons Superior olivary nucleus Intermediate acoustic site Medulla Cochlear nuclei N. Other collaterals go to the vermis of the cerebellum, which is also activated instantaneously in the event of a sudden noise. Third, a high degree of spatial orientation is maintained in the fiber tracts from the cochlea all the way to the cortex. In fact, there are three spatial patterns for termination of the different sound frequencies in the cochlear nuclei, two patterns in the inferior colliculi, one precise pattern for discrete sound frequencies in the auditory cortex, and at least five other less precise patterns in the auditory cortex and auditory association areas. In each of these maps, high-frequency sounds excite neurons at one end of the map, whereas low-frequency sounds excite neurons at the opposite end. The answer, presumably, is that each of the separate areas dissects out some specific feature of the sounds. For example, one of the large maps in the primary auditory cortex almost certainly discriminates the sound frequencies and gives the person the psychic sensation of sound pitches. The frequency range to which each individual neuron in the auditory cortex responds is much narrower than that in the cochlear and brain stem relay nuclei. Yet, by the time the excitation has reached the cerebral cortex, most sound-responsive neurons respond only to a narrow range of frequencies rather than to a broad range. Therefore, somewhere along the pathway, processing mechanisms "sharpen" the frequency response. This sharpening effect is believed to be caused mainly by lateral inhibition, discussed in Chapter 47 in relation to mechanisms for transmitting information in nerves. That is, stimulation of the cochlea at one frequency inhibits sound frequencies on both sides of this primary frequency; this inhibition is caused by collateral fibers angling off the primary signal pathway and exerting inhibitory influences on adjacent pathways. This same effect is important in sharpening patterns of somesthetic images, visual images, and other types of sensations. Many of the neurons in the auditory cortex, especially in the auditory association cortex, do not respond only to specific sound frequencies in the ear. It is believed that these neurons "associate" different sound frequencies with one another or associate sound information with information from other sensory areas of the cortex. For example, an animal that has been trained to recognize a combination or sequence of tones, one following the other in a particular pattern, loses this ability when the auditory cortex is destroyed; furthermore, the animal cannot relearn this type of response. Therefore, the auditory cortex is especially important in the discrimination of tonal and sequential sound patterns. Destruction of one side only slightly reduces hearing in the opposite ear; it does not cause deafness in the ear because of many crossover connections from side to side in the auditory neural pathway. These functions of the auditory association areas and their relation to the overall intellectual functions of the brain are discussed in Chapter 58. The first mechanism functions best at frequencies below 3000 cycles/sec, and the second mechanism operates best at higher frequencies because the head is a greater sound barrier at these frequencies. The time lag mechanism discriminates direction much more exactly than the intensity mechanism because it does not depend on extraneous factors but only on the exact interval of time between two acoustical signals. The Special Senses reaches both ears at exactly the same instant, whereas if the right ear is closer to the sound than the left ear is, the sound signals from the right ear enter the brain ahead of those from the left ear. These two mechanisms cannot tell whether the sound is emanating from in front of or behind the person or from above or below. This discrimination is achieved mainly by the pinnae (the visible outer part), which act as funnels to direct the sound into the two ears. The shape of the pinna changes the quality of the sound entering the ear, depending on the direction from which the sound comes. It changes the quality by emphasizing specific sound frequencies from the different directions. This mechanism for detection of sound direction indicates again how specific information in sensory signals is dissected out as the signals pass through different levels of neuronal activity. In this case, the "quality" of sound direction is separated from the "quality" of sound tones at the level of the superior olivary nuclei.

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Thus erectile dysfunction on coke purchase levitra oral jelly 20mg without prescription, a major cause of decompensated heart failure is failure of the heart to pump sufficient blood to make the kidneys excrete the necessary amounts of fluid every day. Point A on this curve represents the approximate state of the circulation before any compensation has occurred, and point B represents the state a few minutes later, after sympathetic stimulation has compensated as much as it can but before fluid retention has begun. At this time, the cardiac output has risen to 4 L/min and the right atrial pressure has risen to 5 mm Hg. The person appears to be in reasonably good condition, but this state will not remain stable because the cardiac output has not risen high enough to cause adequate kidney excretion of fluid; therefore, fluid retention continues and can eventually be the cause of death. This level is approximately the critical cardiac output level that is required in the average adult person to make the kidneys reestablish normal fluid balance-that is, for the output of salt and water to be as high as the intake of these substances. At cardiac outputs below this level, the fluid-retaining mechanisms discussed in the earlier section remain in play, and the body fluid volume increases progressively. Note again that the cardiac output is still not high enough to cause normal renal output of fluid; therefore, fluid continues to be retained. After another day or so, the right atrial pressure rises to 9 mm Hg, and the circulatory state becomes that depicted by point D. After another few days of fluid retention, the right atrial pressure has risen further but, by now, cardiac function is beginning to decline toward a lower level. It is now clear that further retention of fluid will be more detrimental than beneficial to the circulation. Yet, the cardiac output still is not high enough to bring about normal renal function, so fluid retention not only continues but accelerates because of the falling cardiac output (and the falling arterial pressure that also occurs). Consequently, within a few days, the state of the circulation has reached point F on the curve, with the cardiac output now less than 2. This state has approached or reached incompatibility with life, and the patient will die unless this chain of events can be reversed. This state of heart failure in which the failure continues to worsen is called decompensated heart failure. Clinically, one detects this serious condition of decompensation principally by the progressing edema, especially edema of the lungs, which leads to bubbling rales (a crackling sound) in the lungs and to dyspnea (air hunger). The decompensa- tion process can often be stopped by the following: (1) strengthening the heart in any one of several ways, especially by administering a cardiotonic drug, such as digitalis, so that the heart becomes strong enough to pump adequate quantities of blood required to make the kidneys function normally again; or (2) administering diuretic drugs to increase kidney excretion while at the same time reducing water and salt intake, which results in a balance between fluid intake and output, despite low cardiac output. Both methods stop the decompensation process by reestablishing normal fluid balance so that at least as much fluid leaves the body as enters it. Cardiot- onic drugs, such as digitalis, when administered to a person with a healthy heart, have little effect on increasing the contractile strength of the cardiac muscle. However, when administered to someone with a chronically failing heart, the same drugs can sometimes increase the strength of the failing myocardium by as much as 50% to 100%. Therefore, they are one of the mainstays of therapy in persons with chronic heart failure. Digitalis and other cardiotonic glycosides are believed to strengthen heart contractions by increasing the quantity of calcium ions in muscle fibers. This effect is likely due to inhibition of sodium-potassium adenosine triphosphatase in cardiac cell membranes. Inhibition of the sodium-potassium pump increases the intracellular sodium concentration and slows the sodium-calcium exchange pump, which extrudes calcium from the cell in exchange for sodium. Because the sodium-calcium exchange pump relies on a high sodium gradient across the cell membrane, accumulation of sodium inside the cell reduces its activity. In the failing heart muscle, the sarcoplasmic reticulum fails to accumulate normal quantities of calcium and, therefore, cannot release enough calcium ions into the free fluid compartment of the muscle fibers to cause full contraction of the muscle. The effect of digitalis to depress the sodium-calcium exchange pump and raise calcium Chapter 22 Cardiac Failure ion concentration in cardiac muscle provides the extra calcium needed to increase the muscle contractile force. Therefore, it is usually beneficial to depress the calcium pumping mechanism by a moderate amount using digitalis, allowing the muscle fiber intracellular calcium level to rise slightly. Yet, in a large number of patients, especially those with early acute heart failure, left-sided failure predominates over right-sided failure and, in rare cases, the right side fails without significant failure of the left side. When the left side of the heart fails without concomitant failure of the right side, blood continues to be pumped into the lungs with usual right heart vigor, whereas it is not pumped adequately out of the lungs by the left heart into the systemic circulation. As a result, the mean pulmonary filling pressure rises because of the shift of large volumes of blood from the systemic circulation into the pulmonary circulation. As the volume of blood in the lungs increases, the pulmonary capillary pressure increases and, if this pressure rises above a value approximately equal to the colloid osmotic pressure of the plasma-about 28 mm Hg-fluid begins to filter out of the capillaries into the lung interstitial spaces and alveoli, resulting in pulmonary edema. Thus, the most important problems of left heart failure include pulmonary vascular congestion and pulmonary edema. In severe, acute, left heart failure, pulmonary edema occasionally occurs so rapidly that it can cause death by suffocation in 20 to 30 minutes, discussed later in this chapter. That is, the low arterial pressure that occurs during shock reduces the coronary blood supply even more. This reduction further weakens the heart, which makes the arterial pressure fall further, which makes the shock progressively worse; the process eventually becomes a vicious cycle of cardiac deterioration. In cardiogenic shock caused by myocardial infarction, this problem is greatly compounded by already existing coronary vessel blockage. For example, in a healthy heart, the arterial pressure usually must be reduced below about 45 mm Hg before cardiac deterioration sets in. However, in a heart that already has a blocked major coronary vessel, deterioration begins when the coronary arterial pressure falls below 80 to 90 mm Hg. In other words, even a small decrease in arterial pressure can now set off a vicious cycle of cardiac deterioration. For this reason, in treating myocardial infarction, it is extremely important to prevent even short periods of hypotension. Consequently, the body tissues begin to suffer and even to deteriorate, often leading to death within a few hours to a few days. Even the cardiovascular system suffers from lack of nutrition and deteriorates, along with the remainder of the body, thus hastening death.

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The average diameter of the pulmonary capillaries is only about 5 micrometers erectile dysfunction treatment massage purchase levitra oral jelly with a mastercard, which means that red blood cells must squeeze through them. Factors Affecting Rate of Gas Diffusion Through the Respiratory Membrane Referring to the earlier discussion of diffusion of gases in water, one can apply the same principles to diffusion of gases through the respiratory membrane. Thus, the factors that determine how rapidly a gas will pass through the membrane are the following: (1) the thickness of the membrane; (2) the surface area of the membrane; (3) the diffusion coefficient of the gas in the substance of the membrane; and (4) the partial pressure difference of the gas between the two sides of the membrane. The thickness of the respiratory membrane occasionally increases-for example, as a result of edema fluid in the interstitial space of the membrane and in the alveoli-so the respiratory gases must then diffuse not only through the membrane but also through this fluid. Also, some pulmonary diseases cause fibrosis of the lungs, which can increase the thickness of some portions of the respiratory membrane. Because the rate of diffusion through the membrane is inversely proportional to the thickness of the membrane, any factor that increases the thickness to more than two to three times normal can interfere significantly with normal respiratory exchange of gases. The surface area of the respiratory membrane can be greatly decreased by many conditions. For example, removal of an entire lung decreases the total surface area to half-normal. Also, in emphysema, many of the alveoli coalesce, with dissolution of many alveolar walls. Therefore, the new alveolar chambers are much larger than the original alveoli, but the total surface area of the respiratory membrane is often decreased as much as fivefold because of loss of the alveolar walls. Thus, it is obvious that the alveolar gases are in very close proximity to the blood of the pulmonary capillaries. Furthermore, gas exchange between the alveolar air and pulmonary blood occurs through the membranes of all the terminal portions of the lungs, not merely in the alveoli. All these membranes are collectively known as the respiratory membrane, also called the pulmonary membrane. A layer of fluid containing surfactant that lines the alveolus and reduces the surface tension of alveolar fluid 2. A thin interstitial space between the alveolar epithelium and capillary membrane 516 Chapter 40 Principles of Gas Exchange; Diffusion of Oxygen and Carbon Dioxide Through the Respiratory Membrane substantially impeded, even under resting conditions, and during competitive sports and other strenuous exercise, even the slightest decrease in surface area of the lungs can be a serious detriment to respiratory exchange of gases. The rate of diffusion in the respiratory membrane is almost exactly the same as that in water, for reasons explained earlier. The pressure difference across the respiratory membrane is the difference between the partial pressure of the gas in the alveoli and the partial pressure of the gas in the pulmonary capillary blood. Therefore, the difference between these two pressures is a measure of the net tendency for the gas molecules to move through the membrane. When the partial pressure of a gas in the alveoli is greater than the pressure of the gas in the blood, as is true for O2, net diffusion from the alveoli into the blood occurs. Diffusing capacities for carbon monoxide, oxygen, and carbon dioxide in the normal lungs under resting conditions and during exercise. All the factors discussed earlier that affect diffusion through the respiratory membrane can affect this diffusing capacity. In the average young blood, called the ventilation-perfusion ratio, explained later in this chapter. Therefore, during exercise, oxygenation of the blood is increased not only by increased alveolar ventilation but also by greater diffusing capacity of the respiratory membrane for transporting O2 into the blood. The diffusing man, the diffusing capacity for O2 under resting conditions averages 21 ml/min per mm Hg. The mean O2 pressure difference across the respiratory membrane during normal quiet breathing is about 11 mm Hg. During strenuous exercise or other conditions that greatly increase pulmonary blood flow and alveolar ventilation, the diffusing capacity for O2 increases to about three times the diffusing capacity under resting conditions. Nevertheless, measurements of diffusion of other gases have shown that the diffusing capacity varies directly with the diffusion coefficient of the particular gas. The O2 diffusing capacity can be calculated from measurements of the following: (1) alveolar Po2; (2) Po2 in the pulmonary capillary blood; and (3) the rate of O2 uptake by the blood. Because the blood that perfuses the capillaries is venous blood returning to the lungs from the systemic circulation, it is the gases in this blood with which the alveolar gases equilibrate. In Chapter 41, we describe how the normal venous blood (V) has a Po2 of 40 mm Hg and a Pco2 of 45 mm Hg. Therefore, these are also the normal partial pressures of these two gases in alveoli that have blood flow but no ventilation. This discussion made the assumption that all the alveoli are ventilated equally, and that blood flow through the alveolar capillaries is the same for each alveolus. However, even normally to some extent, and especially in many lung diseases, some areas of the lungs are well ventilated but have almost no blood flow, whereas other areas may have excellent blood flow but little or no ventilation. In either of these conditions, gas exchange through the respiratory membrane is seriously impaired, and the person may suffer severe respiratory distress, despite normal total ventilation and normal total pulmonary blood flow, but with the ventilation and blood flow going to different parts of the lungs. Therefore, a highly quantitative concept has been developed to help us understand respiratory exchange when there is imbalance between alveolar ventilation and alveolar blood flow. At a ratio of eizero perfusion (ther zero or infinity, there is no exchange of gases through the respiratory membrane of the affected alveoli. Therefore, instead of the alveolar gases coming to equilibrium with the venous blood, the alveolar air becomes equal to the humidified inspired air. Furthermore, because normal inspired and humidified air has a Po2 of 149 mm Hg and a Pco2 of 0 mm Hg, these will be the partial pressures of these two gases in the alveoli. Likewise, alveolar Pco2 lies between two extremes; it is normally 40 mm Hg, in contrast to 45 mm Hg in venous blood and 0 mm Hg in inspired air. Thus, under normal conditions, the alveolar air Po2 averages 104 mm Hg and the Pco2 averages 40 mm Hg.

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For example erectile dysfunction medicine list buy levitra oral jelly 20mg mastercard, thrombin has a direct proteolytic effect on prothrombin, tending to convert it into still more thrombin, and it acts on some of the bloodclotting factors responsible for formation of prothrombin activator. Prothrombin activator is generally considered to be formed in two ways, although, in reality, the two ways interact constantly with each other: (1) by the extrinsic pathway that begins with trauma to the vascular wall and surrounding tissues; and (2) by the intrinsic pathway that begins in the blood. In both the extrinsic and the intrinsic pathways, a series of different plasma proteins called blood-clotting factors plays a major role. When converted to the active forms, their enzymatic actions cause the successive, cascading reactions of the clotting process. Most of the clotting factors listed in Table 37-1 are designated by Roman numerals. Extrinsic Pathway for Initiating Clotting the extrinsic pathway for initiating the formation of prothrombin activator begins with a traumatized vascular wall or traumatized extravascular tissues that come in contact with the blood. Traumatized tissue releases a complex of several factors called tissue factor or tissue thromboplastin. This factor is composed especially of phospholipids from the membranes of the tissue plus a lipoprotein complex that functions mainly as a proteolytic enzyme. These mechanisms are set into play by the following: (1) trauma to the vascular wall and adjacent tissues; (2) trauma to the blood; or (3) contact of the blood with damaged endothelial cells or with collagen and other tissue elements outside the blood vessel. In each case, this leads to the formation of prothrombin activator, which then causes prothrombin conversion to thrombin and all the subsequent clotting steps. The activated factor X combines immediately with tissue phospholipids that are part of tissue factors or with additional phospholipids released from platelets, as well as with factor V, to form the complex called prothrombin activator. Within a few seconds, in the presence of Ca2+, prothrombin is split to form thrombin, and the clotting process proceeds as already explained. At first, the factor V in the prothrombin activator complex is inactive, but once clotting begins and thrombin begins to form, the proteolytic action of thrombin activates factor V. This activation then becomes an additional strong accelerator of prothrombin activation. Thus, in the final prothrombin activator complex, activated factor X is the actual protease that causes splitting of prothrombin to form thrombin. Activated factor V greatly accelerates this protease activity, and platelet phospholipids act as a vehicle that further accelerates the process. Note especially the positive feedback effect of thrombin, acting through factor V, to accelerate the entire process once it begins. Intrinsic Pathway for Initiating Clotting the second mechanism for initiating formation of prothrombin activator, and therefore for initiating clotting, begins with trauma to the blood or exposure of the blood to collagen from a traumatized blood vessel wall. Simultaneously, the blood trauma also damages the platelets because of adherence to collagen or to a wettable surface (or by damage in other ways); this releases platelet phospholipids that contain the lipoprotein called platelet factor 3, which also plays a role in subsequent clotting reactions. This reaction also requires high-molecularweight kininogen and is accelerated by prekallikrein. Platelets are the clotting factor that is lacking in the bleeding disease called thrombocytopenia. This step in the intrinsic pathway is the same as the last step in the extrinsic pathway. That is, activated factor X combines with factor V and platelet or tissue phospholipids to form the complex called prothrombin activator. The prothrombin activator, in turn, initiates the cleavage of prothrombin to form thrombin within seconds, thereby setting into motion the final clotting process, as described earlier. The intrinsic pathway is much slower to proceed, usually requiring 1 to 6 minutes to cause clotting. Intravascular Anticoagulants Prevent Blood Clotting in the Normal Vascular System Endothelial Surface Factors. Therefore, in the absence of calcium ions, blood clotting by either pathway does not occur. In the living body, the calcium ion concentration seldom falls low enough to affect blood-clotting kinetics significantly. However, when blood is removed from someone, it can be prevented from clotting by reducing the calcium ion concentration below the threshold level for clotting by deionizing the calcium by causing it to react with substances such as citrate ion or by precipitating the calcium with substances such as oxalate ion. Interaction Between Extrinsic and Intrinsic Pathways-Summary of BloodClotting Initiation It is clear from the schemas of the intrinsic and extrinsic systems that after blood vessels rupture, clotting occurs by both pathways simultaneously. While a clot is forming, about 85% to 90% of the thrombin formed from the prothrombin becomes adsorbed to the fibrin fibers as they develop. This adsorption helps prevent the spread of thrombin into the remaining blood and, therefore, prevents excessive spread of the clot. This further blocks the effect of thrombin on the fibrinogen and then also inactivates thrombin itself during the next 12 to 20 minutes. Heparin is another powerful anticoagulant but, because its concentration in the blood is normally low, it has significant anticoagulant effects only under special physiological conditions. However, heparin is used widely as a pharmacological agent in medical practice in much higher concentrations to prevent intravascular clotting. Heparin is produced by many different cells of the body, but the largest quantities are formed by the basophilic mast cells located in the pericapillary connective tissue throughout the body. These cells continually secrete small quantities of heparin that diffuse into the circulatory system. The basophil cells of the blood, which are functionally almost identical to the mast cells, release small quantities of heparin into the plasma. Mast cells are abundant in tissue surrounding the capillaries of the lungs and, to a lesser extent, capillaries of the liver. It is easy to understand why large quantities of heparin might be needed in these areas because the capillaries of the lungs and liver receive many embolic clots that have formed in slowly flowing venous blood; sufficient production of heparin prevents further growth of the clots. In fact, many small blood vessels in which blood flow has been blocked by clots are reopened by this mechanism.

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This process whereby a pathogen is selected for phagocytosis and destruction is called opsonization erectile dysfunction pills amazon order levitra oral jelly 20 mg amex. The neutrophils are mature cells that can attack and destroy bacteria, even in the circulating blood. Conversely, the tissue macrophages begin life as blood monocytes, which are immature cells while still in the blood and have little ability to fight infectious agents at that time. However, once they enter the tissues, they begin to swell-sometimes increasing their diameters as much as fivefold-to as great as 60 to 80 micrometers, a size that can barely be seen with the naked eye. These cells are now called macrophages, and they are extremely capable of combating disease agents in the tissues. Both neutrophils and macrophages can move through the tissues by ameboid motion, described in Chapter 2. Many different chemical sub- stances in the tissues cause both neutrophils and macrophages to move toward the source of the chemical. When a tissue becomes inflamed, at least a dozen different products that can cause chemotaxis toward the ing the tissues are already mature cells that can immediately begin phagocytosis. On approaching a particle to be phagocytized, the neutrophil first attaches itself to the particle and then projects pseudopodia in all directions around the particle. The lysosomes of macrophages (but not of neutrophils) also contain large amounts of lipases, which digest the thick lipid membranes possessed by some bacteria, such as the tuberculosis bacillus. Phagocytosis of pathogens, such as bacteria, by a phagocytic cell, such as a macrophage. Antibodies coat the bacteria, making them more susceptible to phagocytosis by the macrophage that engulfs the bacterium, bringing it into the cell and forming a phagosome. Lysosomes then attach to the phagosome to form a phagolysosome, which digests the invading pathogen. A single neutrophil can usually phagocytize 3 to 20 bacteria before the neutrophil becomes inactivated and dies. Macrophages are the In addition to the digestion of ingested bacteria in phagosomes, neutrophils and macrophages contain bactericidal agents that kill most bacteria, even when the lysosomal enzymes fail to digest them. This characteristic is especially important because some bacteria have protective coats or other factors that prevent their destruction by digestive enzymes. Much of the killing effect results from several powerful oxidizing agents formed by enzymes in the membrane of the phagosome or by a special organelle called the peroxisome. Also, one of the lysosomal enzymes, myeloperoxidase, catalyzes the reaction between H2O2 and chloride ions to form hypochlorite, which is exceedingly bactericidal. Some bacteria, notably the tuberculosis bacillus, have coats that are resistant to lysosomal digestion and also secrete substances that partially resist the killing effects of the neutrophils and macrophages. However, after entering the tissues and becoming macrophages, another large portion of monocytes becomes attached to the tissues and remains attached for months or even years until they are called on to perform specific local protective functions. They have the same capabilities as the mobile macrophages to phagocytize large quantities of bacteria, viruses, necrotic tissue, or other foreign particles in the tissue. In addition, when appropriately stimulated, they can break away from their attachments and, once again, become mobile macrophages that respond to chemotaxis and all the other stimuli related to the inflammatory process. Thus, the body has a widespread monocyte-macrophage system in virtually all tissue areas. The total combination of monocytes, mobile macrophages, fixed tissue macrophages, and a few specialized endothelial cells in the bone marrow, spleen, and lymph nodes is called the reticuloendothelial system. However, all or almost all these cells originate from monocytic stem end-stage product of monocytes that enter the tissues from the blood. When activated by the immune system, as described in Chapter 35, they are much more powerful phagocytes than neutrophils, often capable of phagocytizing as many as 100 bacteria. Also, after digesting particles, macrophages can extrude the residual products and often survive and function for many more months. Once a foreign particle has been phagocytized, lysosomes and other cytoplasmic granules in the neutrophil or macrophage immediately come into contact with the phagocytic vesicle, and their membranes fuse, thereby dumping many digestive enzymes and bactericidal agents into the vesicle. Thus, the phagocytic vesicle now becomes a digestive vesicle, and digestion of the phagocytized particle begins immediately. Because the term reticuloendothelial system is much better known in medical literature than the term monocytemacrophage system, it should be remembered as a generalized phagocytic system located in all tissues, especially in the tissue areas where large quantities of particles, toxins, and other unwanted substances must be destroyed. Kupffer cells lining the liver sinusoids, showing phagocytosis of India ink particles into the cytoplasm of the Kupffer cells. When infection begins in a subcutaneous tissue and local inflammation ensues, local tissue macrophages can divide in situ and form still more macrophages. Then, they perform the usual functions of attacking and destroying the infectious agents, as described earlier. If the particles are digestible, the macrophages can also digest them and release the digestive products into the lymph. If the particle is not digestible, the macrophages often form a giant cell capsule around the particle until such time-if ever-that it can be slowly dissolved. Such capsules are frequently formed around tuberculosis bacilli, silica dust particles, and even carbon particles. An- late matter that enters the tissues, such as bacteria, can be absorbed directly through the capillary membranes into the blood. Instead, if the particles are not destroyed locally in the tissues, they enter the lymph and flow to the lymph nodes located intermittently along the course of the lymph flow. The foreign particles are then trapped in these nodes in a meshwork of sinuses lined by tissue macrophages.

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Atrial or A- nodal paroxysmal tachycardia impotence kit generic 20 mg levitra oral jelly, both of V which are referred to as supraventricular tachycardias, usually occur in young, otherwise healthy people, and they generally grow out of the predisposition to tachycardia after adolescence. First, this type of tachycardia usually does not occur unless considerable ischemic damage is present in the ventricles. Second, ventricular tachycardia frequently initiates the lethal condition of ventricular fibrillation because of rapid repeated stimulation of the ventricular muscle, as discussed in the next section. Sometimes, intoxication from the heart failure treatment drug digitalis causes irritable foci that lead to ventricular tachycardia. Antiarrhythmic drugs such as amiodarone or lidocaine can be used to treat ventricular tachycardia. In some cases, cardioversion with an electric the most serious of all cardiac arrhythmias is ventricular fibrillation, which, if not stopped within 1 to 3 minutes, is almost invariably fatal. When this phenomenon occurs, many small portions of the ventricular muscle will be contracting at the same time, while equally as many other portions will be relaxing. Thus, there is never a coordinated contraction of all the ventricular muscle at once, which is required for a pumping cycle of the heart. Despite massive movement of stimulatory signals throughout the ventricles, the ventricular chambers neither enlarge nor contract but remain in an indeterminate stage of partial contraction, pumping either no blood or negligible amounts. Therefore, after fibrillation begins, unconsciousness occurs within 4 to 5 seconds because of lack of blood flow to the brain, and irretrievable death of tissues begins to occur throughout the body within a few minutes. Especially likely to initiate fibrillation are sudden electricalshockoftheheart,ischemiaoftheheartmuscle, or ischemia of the specialized conducting system. Therefore, that impulse dies, and the heart awaits a new action potential to begin in the sinus node. Therefore, the following is a more complete explanation of the background conditions that can initiate re-entry and lead to what is referred to as circus movements, which in turn cause ventricular fibrillation. Circus movement, showing annihilation of the impulse in the short pathway and continued propagation of the impulse in the long pathway. A, Initiation of fibrillation in a heart when patches of refractory musculature are present. However, three different conditions can cause this impulse to continue to travel around the circle-that is, cause re- ntry of the e impulse into muscle that has already been excited (circus movement): 1. Thus, in many cardiac disturbances, re-entry can cause abnormal patterns of cardiac contraction or abnormal cardiac rhythms that ignore the pace-setting effects of the sinus node. Instead, they have degenerated into a series of multiple wave fronts that have the appearance of a chain reaction. The first cycle of the electrical stimulus causes a depolarization wave to spread in all directions, leaving all the muscle beneath the electrode in a refractory state. This state of events is depicted in heart A by many lighter patches, which represent excitable cardiac muscle,anddarkpatches,whichrepresentmusclethatis still refractory. Now, continuing 60-cycle stimuli from the electrode can cause impulses to travel only in certain directions through the heart but not in all directions. However, other impulses pass between the refractory areas and continue to travel in the excitable areas. Then, several events transpire in rapid succession, all occurring simultaneously and eventuating in a state of fibrillation. When a depolarization wave reaches a refractory area in the heart, it travels to both sides around the refractory area. Then, when each of these impulses reaches another refractory area, it divides to form two more impulses. In this way, many new wave fronts are continually being formed in the heart by progressive chain reactions until, finally, many small depolarization waves are traveling in many directions at the same time. Furthermore, this irregular pattern of impulse travel causes many circuitous routes for the impulses to travel, greatly lengthening the conductive pathway, which is one of the conditions that sustains the fibrillation. It also results in a continual irregular pattern of patchy refractory areas in the heart. More and more impulses are formed; these impulses cause more and more patches of refractory muscle, and the refractory patches cause more and more division of the impulses. Therefore, whenever a single area of cardiac muscle comes out of refractoriness, an impulse is close at hand to re-enter the area. Here, one can see many impulses traveling in all directions, with some dividing and increasing the number of impulses and others blockedbyrefractoryareas. Asingleelectricshockduring this vulnerable period frequently can lead to an odd pattern of impulses spreading multidirectionally around refractory areas of muscle, which will lead to ventricular fibrillation. Asalreadynoted,becausenopumpingofblood occurs during ventricular fibrillation, this state is lethal unless stopped by successful therapy, such as an immediate electroshock (defibrillation) through the heart, as explained in the next section. This is accomplished by passing intense current through large electrodes placed on two sides of the heart. Allactionpotentials stop, and the heart remains quiescent for 3 to 5 seconds, after which it begins to beat again, usually with the sinus node or some other part of the heart becoming the pacemaker. However,ifthesamere- ntrantfocusthathadorige inally thrown the ventricles into fibrillation is still present, fibrillation may begin again immediately. When electrodes are applied directly to the two sides of the heart, fibrillation can usually be stopped using 1000 volts of direct current applied for a few thousandths of a second. In most cases, defibrillation current is delivered to the heart in biphasic waveforms, alternating the direction of the current pulse through the heart.

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In the brain erectile dysfunction otc treatment purchase levitra oral jelly with a mastercard, the junctions between the capillary endothelial cells are mainly tight junctions that allow only extremely small molecules such as water, oxygen, and carbon dioxide to pass into or out of the brain tissues. In the liver, the clefts between the capillary endothelial cells are nearly wide open so that almost all dissolved substances of the plasma, including the plasma proteins, can pass from the blood into the liver tissues. The pores of the gastrointestinal capillary membranes are midway in size between those of the muscles and those of the liver. When the rate of oxygen usage by the tissue is great- so that tissue oxygen concentration decreases below Chapter 16 the Microcirculation and Lymphatic System: Capillary Fluid Exchange, Interstitial Fluid, and Lymph Flow Arterial end Blood capillary Venous end stituents in the plasma and interstitial fluids that do not readily pass through the capillary membrane. Lipid-Soluble Substances Diffuse Directly Through the Cell Membranes of the Capillary Endothelium. Because these substances can permeate all areas of the capillary membrane, their rates of transport through the capillary membrane are many times faster than the rates for lipid-insoluble substances, such as sodium ions and glucose, which can go only through the pores. Diffusion of fluid molecules and dissolved substances between the capillary and interstitial fluid spaces. This effect, along with multiple other factors that control local tissue blood flow, is discussed in Chapter 17. Despite the fact that blood flow through each capillary is intermittent, so many capillaries are present in the tissues that their overall function becomes averaged. That is, there is an average rate of blood flow through each tissue capillary bed, an average capillary pressure within the capillaries, and an average rate of transfer of substances between the blood of the capillaries and the surrounding interstitial fluid. In the remainder of this chapter, we are concerned with these averages, although it should be remembered that the average functions are, in reality, the functions of billions of individual capillaries, each operating intermittently in response to local conditions in the tissues. Many substances needed by the tissues are soluble in water but cannot pass through the lipid membranes of the endothelial cells; these include water molecules, sodium ions, chloride ions, and glucose. Although only 1/1000 of the surface area of the capillaries is represented by the intercellular clefts between the endothelial cells, the velocity of thermal molecular motion in the clefts is so great that even this small area is sufficient to allow tremendous diffusion of water and water-soluble substances through these cleft pores. To give an idea of the rapidity with which these substances diffuse, the rate at which water molecules diffuse through the capillary membrane is about 80 times greater than the rate at which plasma itself flows linearly along the capillary. That is, the water of the plasma is exchanged with the water of the interstitial fluid 80 times before the plasma can flow the entire distance through the capillary. Electrolytes, nutrients, and waste products of metabolism all diffuse easily through the capillary membrane. The proteins are the only dissolved con- 6 to 7 nanometers, is about 20 times the diameter of the water molecule, which is the smallest molecule that normally passes through the capillary pores. The diameters of plasma protein molecules, however, are slightly greater than the width of the pores. Other substances, such as sodium ions, chloride ions, glucose, and urea, have intermediate diameters. Therefore, the permeability of the capillary pores for different substances varies according to their molecular diameters. Table 16-1 lists the relative permeabilities of the capillary pores in skeletal muscle for various substances, demonstrating, for example, that the permeability for glucose molecules is 0. The capillaries in various tissues have extreme differences in their permeabilities. Also, the permeability of the renal glomerular membrane for water and electrolytes is about 500 times the permeability of the muscle capillaries, but this is not true for the plasma proteins. For these proteins, the capillary permeabilities are very slight, as in other tissues and organs. When we study these different organs later in this text, it should become clear why some tissues require greater degrees of capillary permeability than other tissues. For example, greater degrees of capillary permeability are required for the liver to transfer tremendous amounts of nutrients between the blood and liver parenchymal cells and for the kidneys to allow filtration of large quantities of fluid for the formation of urine. Diffusion Through the Capillary Membrane Is Proportional to the Concentration Difference Between the Two Sides of the Membrane. Proteoglycan filaments are everywhere in the spaces between the collagen fiber bundles. Free fluid vesicles and small amounts of free fluid in the form of rivulets occasionally also occur. It contains two major types of solid structures: (1) collagen fiber bundles; and (2) proteoglycan filaments. They are extremely strong and provide most of the tensional strength of the tissues. The proteoglycan filaments, however, are extremely thin, coiled or twisted molecules composed of about 98% hyaluronic acid and 2% protein. These molecules are so thin that they cannot be seen with a light microscope and are difficult to demonstrate, even with the electron microscope. Nevertheless, they form a mat of very fine reticular filaments aptly described as a brush pile. The fluid in the interstitium is between the concentrations of any given substance on the two sides of the capillary membrane, the greater the net movement of the substance in one direction through the membrane. For example, the concentration of oxygen in capillary blood is normally greater than in the interstitial fluid. Therefore, large quantities of oxygen normally move from the blood toward the tissues.

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Then erectile dysfunction and marijuana cheap levitra oral jelly 20mg line, an additional cylindrical lens is used to correct the remaining error in the remaining plane. To do this, both the axis and the strength of the required cylindrical lens must be determined. Several methods exist for determining the axis of the abnormal cylindrical component of the lens system of an eye. Some of these parallel bars are vertical, some are horizontal, and some are at various angles to the vertical and horizontal axes. After placing various spherical lenses in front of the astigmatic eye, a strength of lens that causes sharp focus of one set of parallel bars but does not correct the fuzziness of the set of bars at right angles to the sharp bars is usually found. It can be shown from the physical principles of optics discussed earlier in this chapter that the axis of the out of focus cylindrical component of the optical system is parallel to the bars that are fuzzy. Once this axis is found, the examiner tries progressively stronger and weaker positive or negative cylindrical lenses, the axes of which are placed in line with the out of focus bars, until the patient sees all the crossed bars with equal clarity. The Special Senses special lens combining both the spherical correction and the cylindrical correction at the appropriate axis. Glass or plastic contact lenses that fit snugly against the anterior surface of the cornea can be inserted. These lenses are held in place by a thin layer of tear fluid that fills the space between the contact lens and the anterior eye surface. A special feature of the contact lens is that it nullifies the refraction that normally occurs at the anterior surface of the cornea almost entirely. This factor is especially important in people whose eye refractive errors are caused by an abnormally shaped cornea, such as those who have an odd-shaped, bulging cornea, a condition called keratoconus. Without the contact lens, the bulging cornea causes such severe abnormality of vision that almost no glasses can correct the vision satisfactorily; when a contact lens is used, however, the corneal refraction is neutralized, and normal refraction by the outer surface of the contact lens is substituted. The contact lens has several other advantages as well, including the following: (1) the lens turns with the eye and gives a broader field of clear vision than glasses; and (2) the contact lens has little effect on the size of the object the person sees through the lens, whereas lenses placed about 1 centimeter in front of the eye do affect the size of the image in addition to correcting the focus. In the early stage of cataract formation, the proteins in some of the lens fibers become denatured. Later, these same proteins coagulate to form opaque areas in place of the normal transparent protein fibers. When a cataract has obscured light transmission so greatly that it seriously impairs vision, the condition can be corrected by surgical removal of the lens. When the lens is removed, the eye loses a large portion of its refractive power, which must be replaced by placing a powerful convex lens in front of the eye; usually, however, an artificial plastic lens is implanted in the eye in place of the removed lens. However, because the lens system of the eye is never perfect, such a retinal spot ordinarily has a total diameter of about 11 micrometers, even with maximal resolution of the normal eye optical system. The average diameter of the cones in the fovea of the retina-the central part of the retina, where vision is most highly developed-is about 1. Nevertheless, because the spot of light has a bright center point and shaded edges, a person can normally distinguish two separate points if their centers lie up to 2 micrometers apart on the retina, which is slightly greater than the width of a foveal cone. The normal visual acuity of the human eye for discriminating between point sources of light is about 25 seconds of arc. That is, when light rays from two separate points strike the eye with an angle of at least 25 seconds between them, they can usually be recognized as two points instead of one. This means that a person with normal visual acuity looking at two bright pinpoint spots of light 10 meters away can barely distinguish the spots as separate entities when they are 1. Outside this foveal area, the visual acuity becomes progressively poorer, decreasing more than 10-fold as the periphery is approached. This is caused by the connection of more and more rods and cones to each optic nerve fiber in the nonfoveal, more peripheral parts of the retina, as discussed in Chapter 52. Chart composed of parallel black bars at different angular orientations for determining the axis of astigmatism. If the person can see well the letters of a size that he or she should be able to see at 20 feet, the person is said to have 20/20 vision-that is, normal vision. If the person can see only letters that he or she should be able to see at 200 feet, the person is said to have 20/200 vision. Perception of distance by the size of the image on the retina (1) and as a result of stereopsis (2). This gives a type of parallax that is always present when both eyes are being used. It is almost entirely this binocular parallax (or stereopsis) that gives a person with two eyes far greater ability to judge relative distances when objects are nearby than a person who has only one eye. However, stereopsis is virtually useless for depth perception at distances beyond 50 to 200 feet. One does not consciously think about the size, but the brain has learned to calculate automatically from image sizes the distances of objects when the dimensions are known. The aqueous humor is a freely flowing fluid, whereas the vitreous humor, sometimes called the vitreous body, is a gelatinous mass held together by a fine fibrillar network composed primarily of greatly elongated proteoglycan molecules. Both water and dissolved substances can diffuse slowly in the vitreous humor, but there is little flow of fluid. The balance between formation and reabsorption of aqueous humor regulates the total volume and pressure of the intraocular fluid. If a person looks off into the distance with the eyes completely still, he or she perceives no moving parallax, but when the person moves the head to one side or the other, the images of nearby objects move rapidly across the retinas, whereas the images of distant objects remain almost completely stationary. For example, by moving the head 1 inch to the side when the object is only 1 inch in front of the eye, the image moves almost all the way across the retinas, whereas the image of an object 200 feet away from the eyes does not move perceptibly. Thus, by using this mechanism of moving parallax, one can tell the relative distances of different objects even though only one eye is used. Essentially all of it is secreted by the ciliary processes, which are linear folds projecting from the ciliary body into the space behind the iris where the lens ligaments and ciliary muscle attach to the eyeball.

Ressel, 54 years: In addition, the blood volume also increases, often by 20% to 30%, and this increase, multiplied by the increased blood hemoglobin concentration, gives an increase in total body hemoglobin of 50% or more. The person is unable to judge texture of materials because this type of judgment depends on highly critical sensations caused by movement of the fingers over the surface to be judged.

Ali, 51 years: Direct destruction of an invading cell by sensitized lymphocytes (cytotoxic T cells). Then, the "normal" opposite kidney retains salt and water because of the renin produced by the ischemic kidney.

Berek, 57 years: Memories are frequently classified according to the type of information that is stored. Thus, as long as the heart is functioning normally, it acts as an automaton, responding to the demands of the tissues.

Gunnar, 64 years: These two mechanisms cannot tell whether the sound is emanating from in front of or behind the person or from above or below. Chapter 8 Excitation and Contraction of Smooth Muscle 0 Millivolts �20 some conditions, and certain types of vascular smooth muscle.

Marius, 48 years: These reservoirs include the following: (1) the spleen, which sometimes can decrease in size sufficiently to release as much as 100 ml of blood into other areas of the circulation; (2) the liver, the sinuses of which can release several hundred milliliters of blood into the remainder of the circulation; (3) the large abdominal veins, which can contribute as much as 300 ml; and (4) the venous plexus beneath the skin, which also can contribute several hundred milliliters. To the left, the ribs during expiration are angled downward, and the external intercostals are elongated forward and downward.

Mufassa, 33 years: This innate immunity makes the human body resistant to diseases such as some paralytic viral infections of animals, hog cholera, cattle plague, and distemper-a viral disease that kills a large percentage of dogs that become afflicted with it. The blood pressure in the vessels causes them to dilate and pulsate intensely, and it is postulated that the excessive stretching of the walls of the arteries-including some extracranial arteries, such as the temporal artery-causes the actual pain of migraine headaches.