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This action potential in turn causes electrical current to flow along both the outside and the inside of the fiber and initiates additional action potentials erectile dysfunction for young adults buy erectafil without a prescription. This process continues again and again until the nerve signal goes all the way to the end of the fiber. In each case in which positive feedback is useful, the positive feedback is part of an overall negative feedback process. For example, in the case of blood clotting, the positive feedback clotting process is a negative feedback process for maintenance of normal blood volume. Also, the positive feedback that causes nerve signals allows the nerves to participate in thousands of negative feedback nervous control systems. For instance, some movements of the body occur so 9 Unit I Introduction to Physiology: the Cell and General Physiology rapidly that there is not enough time for nerve signals to travel from the peripheral parts of the body all the way to the brain and then back to the periphery again to control the movement. Therefore, the brain uses a principle called feed-forward control to cause required muscle contractions. That is, sensory nerve signals from the moving parts apprise the brain whether the movement is performed correctly. If not, the brain corrects the feedforward signals that it sends to the muscles the next time the movement is required. Then, if still further correction is necessary, this process will be performed again for subsequent movements. Therefore, a major share of this text is devoted to discussing these life-giving mechanisms. To summarize, the body is actually a social order of about 100 trillion cells organized into different functional structures, some of which are called organs. Each functional structure contributes its share to the maintenance of homeostatic conditions in the extracellular fluid, which is called the internal environment. As long as normal conditions are maintained in this internal environment, the cells of the body continue to live and function properly. Each cell benefits from homeostasis, and in turn, each cell contributes its share toward the maintenance of homeostasis. To understand the function of organs and other structures of the body, it is essential that we first understand the basic organization of the cell and the functions of its component parts. These proteins can be divided into two types: structural proteins and functional proteins. Structural proteins are present in the cell mainly in the form of long filaments that are polymers of many individual protein molecules. A prominent use of such intracellular filaments is to form microtubules that provide the "cytoskeletons" of such cellular organelles as cilia, nerve axons, the mitotic spindles of cells undergoing mitosis, and a tangled mass of thin filamentous tubules that hold the parts of the cytoplasm and nucleoplasm together in their respective compartments. Fibrillar proteins are found outside the cell, especially in the collagen and elastin fibers of connective tissue and in blood vessel walls, tendons, ligaments, and so forth. The functional proteins are an entirely different type of protein and are usually composed of combinations of a few molecules in tubular-globular form. These proteins are mainly the enzymes of the cell and, in contrast to the fibrillar proteins, are often mobile in the cell fluid. The enzymes come into direct contact with other substances in the cell fluid and catalyze specific intracellular chemical reactions. For instance, the chemical reactions that split glucose into its component parts and then combine these with oxygen to form carbon dioxide and water while simultaneously providing energy for cellular function are all catalyzed by a series of protein enzymes. Lipids are several types of substances that are grouped together because of their common property of being soluble in fat solvents. Especially important lipids are phospholipids and cholesterol, which together constitute only about 2 percent of the total cell mass. The significance of phospholipids and cholesterol is that they are mainly insoluble in water and therefore are used to form the cell membrane and intracellular membrane barriers that separate the different cell compartments. The nucleus is separated from the cytoplasm by a nuclear membrane, and the cytoplasm is separated from the surrounding fluids by a cell membrane, also called the plasma membrane. The different substances that make up the cell are collectively called protoplasm. Protoplasm is composed mainly of five basic substances: water, electrolytes, proteins, lipids, and carbohydrates. The principal fluid medium of the cell is water, which is present in most cells, except for fat cells, in a concentration of 70 to 85 percent. Chemical reactions take place among the dissolved chemicals or at the surfaces of the suspended particles or membranes. Important ions in the cell include potassium, magnesium, phosphate, sulfate, bicarbonate, and smaller quantities of sodium, chloride, and calcium. These ions are all discussed in more detail in Chapter 4, which considers the interrelations between the intracellular and extracellular fluids. The ions provide inorganic chemicals for cellular reactions and also are necessary for operation of some of the cellular control mechanisms. For instance, ions acting at 11 Unit I Introduction to Physiology: the Cell and General Physiology Cell membrane Cytoplasm Nucleolus Nuclear membrane Nucleoplasm Nucleus water is not soluble in lipids. However, protein molecules in the membrane often penetrate all the way through the membrane, thus providing specialized pathways, often organized into actual pores, for passage of specific substances through the membrane. Also, many other membrane proteins are enzymes that catalyze a multitude of different chemical reactions, discussed here and in subsequent chapters.

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However erectile dysfunction treatment options in india purchase erectafil 20 mg on-line, this is not the usual case because the septum and other endocardial areas have a longer period of contraction than do 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 rela tively small because the area of repolarization is small. Finally, the vector becomes weaker again because the areas of depolarization still per sisting 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 polar ized 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 depolariza tion signal. Therefore, the musculature around the sinus node becomes depolarized a long time before the muscu lature 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. Thus, when repolarization begins, the region around the sinus node becomes positive with respect to the remainder of the atria. Therefore, the atrial repolariza tion 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. It changes in two aspects: 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 vecto rial electrical potential. However, as soon as current begins to flow through the ventricles at the beginning of ventricu lar 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. Vector cardiograms can be recorded on an oscilloscope by con necting body surface electrodes from the neck and lower abdomen to the vertical plates of the oscilloscope and con necting chest surface electrodes from each side of the heart to the horizontal plates. When the vector changes, the spot of light on the oscilloscope follows the course of the posi tive end of the changing vector, thus inscribing the vector cardiogram on the oscilloscopic screen. Note from this vectorcardiogram that the preponderant direction of the vectors of the ven tricles during depolarization is mainly toward the apex of the heart. That is, during most of the cycle of ventricular depolarization, the direction of the electrical potential (negative to positive) is from the base of the ventricles toward the apex. This preponderant direction of the potential during depolarization 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 devia tion beyond the normal limits, as follows. If the net potential of lead I is positive, it is plotted in a positive direction along the line depicting lead I. If the heart is angulated to the left, the mean electrical axis of the heart also shifts to the left. Such shift occurs (1) at the end of deep expiration, (2) when a person lies down, because the abdominal contents press upward against the diaphragm, and (3) quite frequently in obese people whose diaphragms normally press upward against the heart all the time as a result of increased visceral adiposity. Likewise, angulation of the heart to the right causes the mean electrical axis of the ventricles to shift to the right. This shift occurs (1) at the end of deep inspiration, (2) when a person stands up, and (3) normally in tall, lanky people whose hearts hang downward. When one ventricle greatly hypertrophies, the axis of the heart shifts toward the hypertrophied ventricle for two reasons. First, a greater quantity of muscle exists on the hypertrophied side of the heart than on the other side, which allows generation of greater electrical potential on that side. Second, more time is required for the depolarization wave to travel through the hypertrophied ventricle than through the normal ventricle.

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Therefore erectile dysfunction pills for high blood pressure erectafil 20 mg with visa, the elongated muscle on one side of a joint can contract with far greater force than the shorter muscle on the opposite side. As an arm or leg moves toward its midposition, the strength of the longer muscle decreases, whereas the strength of the shorter muscle increases until the two strengths equal each other. Thus, by varying the ratios of the degree of activation of the agonist and antagonist muscles, the nervous system directs the positioning of the arm or leg. We learn in Chapter 55 that the motor nervous system has additional important mechanisms to compensate for different muscle loads when directing this positioning process. Their diameters, lengths, strengths, and vascular supplies are altered, and even the types of muscle fibers are altered at least slightly. Indeed, experiments in animals have shown that muscle contractile proteins in some smaller, more active muscles can be replaced in as little as 2 weeks. Virtually all muscle hypertrophy results from an increase in the number of actin and myosin filaments in each muscle fiber, causing enlargement of the individual muscle fibers; this condition is called simply fiber hypertrophy. Hypertrophy occurs to a much greater extent when the muscle is loaded during the contractile process. Only a few strong contractions each day are required to cause significant hypertrophy within 6 to 10 weeks. It is known, however, that the rate of synthesis of muscle contractile proteins is far greater when hypertrophy is developing, leading also to progressively greater numbers of both actin and myosin filaments in the myofibrils, often increasing as much as 50 percent. In turn, some of the myofibrils themselves have been observed to split within hypertrophying muscle to form new myofibrils, but the importance of this process in usual muscle hypertrophy is still unknown. Along with the increasing size of myofibrils, the enzyme systems that provide energy also increase. This increase is especially true of the enzymes for glycolysis, allowing rapid supply of energy during short-term forceful muscle contraction. When a muscle remains unused for many weeks, the rate of degradation of the contractile proteins is more rapid than the rate of replacement. Proteasomes are large protein complexes that degrade damaged or unneeded proteins by proteolysis, a chemical reaction that breaks peptide bonds. Ubiquitin is a regulatory protein that basically labels which cells will be targeted for proteosomal degradation. Another type of hyper- added as rapidly as several per minute in newly developing muscle, illustrating the rapidity of this type of hypertrophy. Conversely, when a muscle continually remains shortened to less than its normal length, sarcomeres at the ends of the muscle fibers can actually disappear. It is by these processes that muscles are continually remodeled to have the appropriate length for proper muscle contraction. When it does occur, the mechanism is linear splitting of previously enlarged fibers. When a muscle loses its nerve supply, it no longer receives the contractile signals that are required to maintain normal muscle size. After about 2 months, degenerative changes also begin to appear in the muscle fibers. If the nerve supply to the muscle grows back rapidly, full return of function can occur in as little as 3 months, but from that time onward, the capability of functional return becomes less and less, with no further return of function after 1 to 2 years. In the final stage of denervation atrophy, most of the muscle fibers are destroyed and replaced by fibrous and fatty tissue. The fibers that do remain are composed of a long cell membrane with a lineup of muscle cell nuclei but with few or no contractile properties and little or no capability of regenerating myofibrils if a nerve does regrow. The fibrous tissue that replaces the muscle fibers during denervation atrophy also has a tendency to continue shortening for many months, which is called contracture. Therefore, one of the most important problems in the practice of physical therapy is to keep atrophying muscles from developing debilitating and disfiguring contractures. This goal is achieved by daily stretching of the muscles or use of appliances that keep the muscles stretched during the atrophying process. When some but not trophy occurs when muscles are stretched to greater than normal length. This stretching causes new sarcomeres to be added at the ends of the muscle fibers, where they attach to the tendons. In fact, new sarcomeres can be all nerve fibers to a muscle are destroyed, as commonly occurs in poliomyelitis, the remaining nerve fibers branch off to form new axons that then innervate many of the paralyzed muscle fibers. This process results in large motor units called macromotor units, which can contain as many as five times the normal number of muscle fibers for each motoneuron coming from the spinal cord. The formation of large motor units decreases the fineness of control one has over the muscles but does allow the muscles to regain varying degrees of strength. Several hours after death, all the muscles of the body go into a state of contracture called "rigor mortis"; that is, the muscles contract and become rigid, even without action potentials. The muscles remain in rigor until the muscle proteins deteriorate about 15 to 25 hours later, which presumably results from autolysis caused by enzymes released from lysosomes. The muscular dystrophies include several inherited disorders that cause progressive weakness and degeneration of muscle fibers, which are replaced by fatty tissue and collagen. This disease affects only males because it is transmitted as an X-linked recessive trait and is caused by a mutation of the gene that encodes for a protein called dystrophin, which links actins to proteins in the muscle cell membrane. Dystrophin and associated proteins form an interface between the intracellular contractile apparatus and the extracellular connective matrix. Although the precise functions of dystrophin are not completely understood, lack of dystrophin or mutated forms of the protein cause muscle cell membrane destabilization, activation of multiple pathophysiological processes, including altered intracellular calcium handling, and impaired membrane repair after injury.

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Oxygen is one of the metabolic nutrients required to cause vascular muscle contraction (with other nutrients required as well) erectile dysfunction signs erectafil 20 mg purchase mastercard. Therefore, in the absence of adequate oxygen, it is reasonable to believe that the blood vessels would relax and therefore dilate. Also, increased utilization of oxygen in the tissues as a result of increased metabolism theoretically could decrease the availability of oxygen to the smooth muscle fibers in the local blood vessels, and this decreased availability, too, would cause local vasodilation. This figure shows a tissue unit, consisting of a metarteriole with a single sidearm capillary and its surrounding tissue. At the origin of the capillary is a precapillary sphincter, and around the metarteriole are several other smooth muscle fibers. The number of precapillary sphincters that are open at any given time is roughly proportional to the requirements of the tissue for nutrition. The precapillary sphincters and metarterioles open and close cyclically several times per minute, with the duration of the open phases being proportional to the metabolic needs of the tissues for oxygen. Because smooth muscle requires oxygen to remain contracted, one might assume that the strength of contraction of the sphincters would increase with an increase in oxygen concentration. Consequently, when the oxygen concentration in the tissue rises above a certain level, the precapillary and metarteriole sphincters presumably would close until the tissue cells consume the excess oxygen. However, when the excess oxygen is gone and the oxygen concentration falls low enough, the sphincters would open once more to begin the cycle again. Thus, on the basis of available data, either a vasodilator substance theory or an oxygen demand theory could explain acute local blood flow regulation in response to the metabolic needs of the tissues. It also is possible that this same effect occurs when other nutrients, such as amino acids or fatty acids, are deficient, although this issue has not been studied adequately. In addition, vasodilation occurs in the vitamin deficiency disease beriberi, in which the patient has deficiencies of the vitamin B substances thiamine, niacin, and riboflavin. In this disease, the peripheral vascular blood flow almost everywhere in the body often increases twofold to threefold. Reactive hyperemia is another manifestation of the local "metabolic" blood flow regulation mechanism; that is, lack of flow sets into motion all of the factors that cause vasodilation. After short periods of vascular occlusion, the extra blood flow during the reactive hyperemia phase lasts long enough to repay almost exactly the tissue oxygen deficit that has accrued during the period of occlusion. This mechanism emphasizes the close connection between local blood flow regulation and delivery of oxygen and other nutrients to the tissues. When any tissue becomes highly active, Special Examples of Acute "Metabolic" Control of Local Blood Flow the mechanisms we have described thus far for local blood flow control are called "metabolic mechanisms" because all of them function in response to the metabolic needs of the tissues. The increase in local metabolism causes the cells to devour tissue fluid nutrients rapidly and also to release large quantities of vasodilator substances. In this way, the active tissue receives the additional nutrients required to sustain its new level of function. As pointed out earlier, active hyperemia in skeletal muscle can increase local muscle blood flow as much as 20-fold during intense exercise. Autoregulation of Blood Flow During Changes in Arterial Pressure-"Metabolic" and "Myogenic" Mechanisms In any tissue of the body, a rapid increase in arterial pressure causes an immediate rise in blood flow. However, within less than a minute, the blood flow in most tissues returns almost to the normal level, even though the arterial pressure is kept elevated. Note that between arterial pressures of about 70 mm Hg and 175 mm Hg the blood flow increases only 20 to 30 percent even though the arterial pressure increases 150 percent. In some tissues, such as the brain and the heart, this autoregulation is even more precise. For almost a century, two views have been proposed to explain this acute autoregulation mechanism. The metabolic theory can be understood easily by applying the basic principles of local blood flow regulation discussed in previous sections. Indeed, metabolic factors appear to override the myogenic mechanism in circumstances in which the metabolic demands of the tissues are significantly increased, such as during vigorous muscle exercise, which can cause dramatic increases in skeletal muscle blood flow. All mechanisms are discussed throughout this text in relation to specific organs, but two notable mechanisms are as follows: 1. In the kidneys, blood flow control is vested to a great extent in a mechanism called tubuloglomerular feedback, in which the composition of the fluid in the early distal tubule is detected by an epithelial structure of the distal tubule itself called the macula densa. This structure is located where the distal tubule lies adjacent to the afferent and efferent arterioles at the nephron juxtaglomerular apparatus. When too much fluid filters from the blood through the glomerulus into the tubular system, feedback signals from the macula densa cause constriction of the afferent arterioles, in this way reducing both renal blood flow and glomerular filtration rate back to nearly normal. In the brain, in addition to control of blood flow by tissue oxygen concentration, the concentrations of carbon dioxide and hydrogen ions play prominent roles. An increase of either or both of these ions dilates the cerebral vessels and allows rapid washout of the excess carbon dioxide or hydrogen ions from the brain tissues. This mechanism is important because the level of excitability of the brain itself is highly dependent on exact control of both carbon dioxide concentration and hydrogen ion concentration. This special mechanism for cerebral blood flow control is presented in Chapter 62. In the skin, blood flow control is closely linked to regulation of body temperature. Cutaneous and subcutaneous flow regulates heat loss from the body by metering the flow of heat from the core to the surface of the body, where heat is lost to the environment. Skin blood flow is controlled largely by the central nervous system through the sympathetic nerves, as discussed in Chapter 74. Although skin blood flow is only about 3 ml/min/100 g of tissue in cool weather, large changes from that value can occur as needed. When humans are exposed to body heating, skin blood flow may increase manyfold, to as high as 7 to 8 L/min for the entire body.

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The cholesterol molecules in the membrane are also lipids because their steroid nuclei are highly fat soluble erectile dysfunction viagra dosage best erectafil 20 mg. They mainly help determine the degree of permeability (or impermeability) of the bilayer to water-soluble constituents of body fluids. There are two types of cell membrane proteins: integral proteins that protrude all the way through the membrane and peripheral proteins that are attached only to one surface of the membrane and do not penetrate all the way through. Many of the integral proteins provide structural chan nels (or pores) through which water molecules and watersoluble substances, especially ions, can diffuse between the extracellular and intracellular fluids. These protein channels also have selective properties that allow preferential diffusion of some substances over others. Other integral proteins act as carrier proteins for transporting substances that otherwise could not penetrate the lipid bilayer. Sometimes these carrier proteins even transport substances in the direction opposite to their electrochemical gradients for diffusion, which is called "active transport. Integral membrane proteins can also serve as recep tors for water-soluble chemicals, such as peptide hormones, that do not easily penetrate the cell membrane. Interaction of cell membrane receptors with specific ligands that bind to the receptor causes conformational changes in the receptor protein. This process, in turn, enzymatically activates the intracellular part of the protein or induces interactions between the receptor and proteins in the cytoplasm that act as second messengers, relaying the signal from the extracellular part of the receptor to the interior of the cell. In this way, integral proteins spanning the cell membrane provide a means of conveying information about the environment to the cell interior. These peripheral proteins function almost entirely as enzymes or as controllers of transport of substances through the cell membrane "pores. In fact, most of the integral proteins are glycoproteins, and about one tenth of the membrane lipid molecules are glycolipids. The "glyco" portions of these molecules almost invariably protrude to the outside of the cell, dangling outward from the cell surface. Many other carbohydrate compounds, called proteoglycans-which are mainly carbohydrate substances bound to small protein cores-are loosely attached to the outer surface of the cell as well. Thus, the entire outside surface of the cell often has a loose carbohydrate coat called the glycocalyx. The carbohydrate moieties attached to the outer surface of the cell have several important functions: 1. Many of them have a negative electrical charge, which gives most cells an overall negative surface charge that repels other negatively charged objects. The glycocalyx of some cells attaches to the glycocalyx of other cells, thus attaching cells to one another. Many of the carbohydrates act as receptor sub stances for binding hormones, such as insulin; when 14 bound, this combination activates attached internal proteins that, in turn, activate a cascade of intracellular enzymes. Some carbohydrate moieties enter into immune reactions, as discussed in Chapter 35. The jelly-like fluid portion of the cytoplasm in which the particles are dispersed is called cytosol and contains mainly dissolved proteins, electrolytes, and glucose. Dispersed in the cytoplasm are neutral fat globules, glycogen granules, ribosomes, secretory vesicles, and five especially important organelles: the endoplasmic reticu lum, the Golgi apparatus, mitochondria, lysosomes, and peroxisomes. Also, their walls are constructed of lipid bilayer membranes that contain large amounts of proteins, similar to the cell membrane. The total surface area of this structure in some cells-the liver cells, for instance-can be as much as 30 to 40 times the cell membrane area. The space inside the tubules and vesicles is filled with endo plasmic matrix, a watery medium that is different from the fluid in the cytosol outside the endoplasmic reticulum. Electron micrographs show that the space inside the endoplasmic reticulum is connected with the space between the two membrane surfaces of the nuclear membrane. Substances formed in some parts of the cell enter the space of the endoplasmic reticulum and are then directed to other parts of the cell. Also, the vast surface area of this reticulum and the multiple enzyme systems attached to its membranes provide machinery for a major share of the metabolic functions of the cell. The agranular reticulum functions for the synthesis of lipid substances and for other processes of the cells promoted by intrareticular enzymes. The Golgi apparatus is usually composed of four or more stacked layers of thin, flat, enclosed vesicles lying near one side of the nucleus. This apparatus is prominent in secretory cells, where it is located on the side of the cell from which the secretory substances are extruded. The transported substances are then processed in the Golgi apparatus to form lysosomes, secretory vesicles, and other cytoplasmic components that are discussed later in this chapter. Attached to the outer surfaces of many parts of the endoplasmic reticulum are large numbers of minute granular particles called ribosomes. Where these particles are present, the reticulum is called the granular endoplasmic reticulum. The lysosomes provide an intracellular digestive system that allows the cell to digest (1) damaged cellular structures, (2) food particles that have been ingested by the cell, and (3) unwanted matter such as bacteria. The lysosome is quite different in various cell types, but it is usually 250 to 750 nanometers in diameter. It is surrounded by a typical lipid 15 plasmic reticulum has no attached ribosomes. This part Unit I Introduction to Physiology: the Cell and General Physiology bilayer membrane and is filled with large numbers of small granules 5 to 8 nanometers in diameter, which are protein aggregates of as many as 40 different hydrolase (digestive) enzymes. A hydrolytic enzyme is capable of splitting an organic compound into two or more parts by combining hydrogen from a water molecule with one part of the compound and combining the hydroxyl portion of the water molecule with the other part of the compound.

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Muscular branches are distributed to biceps femoris discount erectile dysfunction pills purchase 20 mg erectafil, semitendinosus, semimembranosus and the ischial part of adductor magnus. The point of division of the sciatic nerve into its tibial and common fibular components is very variable. The common site is at the junction of the middle and lower thirds of the thigh, near the apex of the popliteal fossa, but the division may occur at any level above this point and, rarely, may occur below it. On rare occasions, it is supplied by branches from the superior gluteal or internal pudendal arteries, which reach the nerve on its medial side. Lower in the thigh, arterial branches derived from the perforating branches of the profunda femoris artery or the anastomotic chain between them or, occasionally, from the popliteal artery, enter the nerve on its lateral or anterolateral side (Sunderland 1945). The numerous arterial branches to the sciatic nerve anastomose with each other to form extraneural and intraneural arterial chains (Sunderland 1945, Ugrenovic et al 2013). Lateral dorsal cutaneous nerve Medial and lateral plantar nerves 80 Pelvic girdle, gluteal region and thigh sciatic nerve palsy is very rare. As it leaves the pelvis, it passes either behind piriformis or sometimes through the muscle, and at that point it may very rarely become entrapped or tethered; the piriformis syndrome is a controversial condition in which an anomalous relationship between piriformis and the sciatic nerve is thought to cause pain in the buttocks and along the course of the sciatic nerve. However, the most common cause of serious sciatic nerve injury (and of the resulting major medicolegal claims) is iatrogenic (Dillow et al 2013). The nerve may be damaged in misplaced therapeutic injections into gluteus maximus. Sciatic nerve palsy occurs after total hip replacement or similar surgery in 1% of cases, and may be caused by sharp injury, burning from bone cement, traction from instruments, manipulation of the hip, inadvertent lengthening of the femur, or haematoma surrounding the nerve. For some reason, possibly anatomical, the common fibular component of the sciatic nerve is more usually affected; the patient has a foot drop and a high-stepping gait. Nerve to obturator internus the nerve to obturator internus arises from the ventral branches of the fifth lumbar and first and second sacral ventral rami. It leaves the pelvis via the greater sciatic foramen below piriformis, supplies a branch to the upper posterior surface of gemellus superior, crosses the ischial spine lateral to the internal pudendal vessels, re-enters the pelvis via the lesser sciatic foramen, and enters the pelvic surface of obturator internus. Posterior femoral cutaneous nerve (posterior cutaneous nerve of the thigh) the posterior femoral cutaneous nerve (posterior cutaneous nerve of the thigh) arises from the dorsal branches of the first and second, and the ventral branches of the second and third sacral rami. It descends in the back of the thigh superficial to the long head of biceps femoris, deep to the fascia lata. It pierces the deep fascia behind the knee and accompanies the short saphenous vein to mid-calf, its terminal twigs connecting with the sural nerve. Its branches are cutaneous and are distributed to the gluteal region, perineum, posterior thigh and proximal posterior leg. Three or four gluteal branches (inferior clunial nerves) curl round the lower border of gluteus maximus to supply the skin over the inferolateral portion of the muscle. The perineal branch supplies the superomedial skin in the thigh, curves forwards across the hamstrings below the ischial tuberosity, pierces the fascia lata and then runs in the superficial perineal fascia to the scrotal or labial skin. It communicates with the inferior rectal and posterior scrotal or labial branches of the perineal nerve, and gives numerous branches to the skin of the back and medial side of the thigh, the popliteal fossa and the proximal part of the back of the leg. One study found the perineal branch of the posterior cutaneous nerve of the thigh in about one-half of specimens (Tubbs et al 2009). Inferior gluteal nerve the inferior gluteal nerve arises from the dorsal branches of the fifth lumbar and first and second sacral ventral rami. Superior gluteal nerve the superior gluteal nerve arises from the dorsal branches of the fourth and fifth lumbar and first sacral ventral rami. The superior branch accompanies the upper branch of the deep division of the superior gluteal artery to supply gluteus medius and occasionally gluteus minimus. The inferior branch runs with the lower ramus of the deep division of the superior gluteal artery across gluteus minimus, supplies the glutei medius and minimus, and ends in tensor fasciae latae. Nerve to piriformis the nerve to piriformis usually arises from the dorsal branches of the first and second sacral ventral rami (sometimes only the second) and enters the anterior surface of piriformis. Perforating cutaneous nerve the perforating cutaneous nerve usually arises from the posterior aspects of the second and third sacral ventral spinal rami. It pierces the sacrotuberous ligament, curves round the inferior border of gluteus maximus and supplies the skin over the inferomedial aspect of this muscle. The nerve may arise from the pudendal nerve or it may be absent, in which case it may be replaced either by a branch from the posterior femoral cutaneous nerve or from the third and fourth, or fourth and fifth, sacral ventral rami. Visceral and pelvic muscular branches of sacral plexus Visceral branches of the sacral plexus are described on page 1229. Nerve to quadratus femoris the nerve to quadratus femoris arises from the ventral branches of the fourth lumbar to the first sacral ventral rami. It leaves the pelvis via the greater sciatic foramen below piriformis, descends on the ischium deep to the sciatic nerve, the gemelli and the tendon of obturator internus, and supplies gemellus inferior, quadratus femoris and the hip joint. Gilligan I, Chandraphak S, Mahakkanukrauh P 2013 Femoral neck-shaft angle in humans: variation relating to climate, clothing, lifestyle, sex, age and side. A detailed study of the variations in the origin of the deep femoral artery and lateral and medial circumflex arteries in 100 thighs. A neglected and original work with detailed information on the blood supply of the sciatic nerve. A recent and original study on the perineal branch of the posterior femoral cutaneous nerve.

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They are irregular in outline and lie within the perisinusoidal space of Disse between the sinusoids and the hepatocyte plates impotence with diabetes cheap erectafil online american express. They are thought to be mesenchymal in origin and are characterized by numerous cytoplasmic lipid droplets. They store the fat-soluble vitamin A in their lipid droplets and are a significant source of growth factors involved in liver Hepatic stem cells Hepatic stem cells are undifferentiated, pluripotential cells and are understood to reside around the canals of Hering; they are derived from the ductal plate in fetal livers. Their role in iron metabolism is reflected by the presence of storage vacuoles containing crystals of ferritin and haemosiderin. The surfaces of hepatocytes facing the sinusoids exhibit numerous microvilli, approximately 0. Lateral plasma membranes of adjacent hepatocytes form microscopic channels, the bile canaliculi, which are specialized regions of intercellular space formed by apposing grooves in hepatocyte plasma membranes, sealed from extraneous interstitial space by tight junctions. Individual tight junction complexes, either alone or in combination, are involved in signalling pathways in health and disease. Numerous membranebound exocytotic vesicles cluster near the lumen of the canaliculi because the secretion of bile is targeted at the canalicular plasma membrane. Hepatic stellate cells also play a major role in pathological processes (Yin et al 2013). In response to liver damage, they become activated and predominantly myofibroblast-like. They are responsible for the replacement of damaged hepatocytes with collagenous scar tissue, a process called hepatic fibrosis, that is seen initially in zone 3, around central veins. Fibrosis can progress to cirrhosis, where the parenchymal architecture and pattern of blood flow within the liver are destroyed, with major systemic consequences. Sinusoidal endothelial cells Hepatic venous sinusoids are generally wider than blood capillaries and are lined by a thin but highly fenestrated endothelium that lacks a basal lamina. The endothelial cells are typically flattened, each with a central nucleus, and are joined to each other by junctional complexes. The fenestrae are grouped in clusters with a mean diameter of 100 nm, allowing plasma direct access to the basal plasma membranes of hepatocytes. Kupffer cells Kupffer cells are hepatic macrophages derived from circulating blood monocytes and originate in the bone marrow. They are long-term hepatic residents and lie within the sinusoidal lumen attached to the endothelial surface. Kupffer cells are irregular in shape and have long processes that extend into the sinusoidal lumen. They form a major part of the mononuclear phagocyte system, which is responsible for removing cellular and microbial debris from the circulation, and for secreting cytokines involved in defence. They remove aged and damaged red cells from the hepatic circulation, a function normally shared with the spleen but fulfilled entirely by the liver after splenectomy. Takasaki K, Koabayashi S, Tanaka S et al 1986 Highly selected hepatic resection by Glissonian sheath-binding method. Terminology Committee of the International Hepato-Pancreato-Biliary Association 2000 the Brisbane 2000 terminology of liver anatomy and resections. Hribernik M, Trotovsek B 2014 Intrahepatic venous anastomoses with a focus on the middle hepatic vein anastomoses in normal human livers: anatomical study on liver corrosion casts. Makuuchi M 2013 Could we or should we replace the conventional nomenclature of liver resections A concise illustrated account of the derivation and individuals behind the more common eponyms associated with liver anatomy and surgery. Yamamoto M, Katagiri S, Ariizumi S et al 2012 Glissonean pedicle transection method for liver surgery (with video). The intrahepatic ducts are formed from bile ductules that join to form segmental ducts. In the adult, the gallbladder is between 7 and 10 cm long, with a resting volume of about 25 ml and a capacity of up to 50 ml (Di Ciaula et al 2012). It usually lies in a shallow fossa (the gallbladder bed) on the visceral surface of the right lobe of the liver, covered by peritoneum continued from the liver surface. Rarely, the gallbladder is almost completely buried within the liver (intrahepatic gallbladder; Guiteau et al 2009), or suspended from the liver by a peritoneal mesentery (when it is at risk of torsion; Gupta et al 2009), or connected to the duodenum by an extension of the free edge of the lesser omentum (cystoduodenal ligament; Ashaolu et al 2011). The neck lies at the medial end, close to the porta hepatis, and almost always has a short peritoneal attachment (mesentery) to the liver, which usually contains the cystic artery. The mucosa at the medial end of the neck is obliquely ridged, forming a crescentic fold that is continuous with the spirally arranged mucosal folds in the cystic duct (Dasgupta and Stringer 2005). The body of the gallbladder normally lies in contact with the visceral surface of the liver. When the neck possesses a mesentery, this rapidly shortens along the length of the body as it lies in the gallbladder fossa. The body lies anterior to the second part of the duodenum and the right end of the transverse colon. The bulbous fundus lies at the lateral end of the body and usually projects past the inferior border of the liver to a variable extent.

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Conversely impotence biking order erectafil 20 mg line, the pyrimidines inhibit their own enzymes but activate the purine enzymes. In this way, there is continual cross-feed between the synthesizing systems for these two substances, resulting in almost exactly equal amounts of the two substances in the cells at all times. This uncoiling is achieved by enzymes that periodically cut each helix along its entire length, rotate each segment enough to cause separation, and then resplice the helix. Even during this period, preliminary changes that will lead to the mitotic process are beginning to take place. Because of repair and proofreading, mistakes are rarely made in the transcription process. The mutation causes formation of some abnormal protein in the cell rather than a needed protein, often leading to abnormal cellular function and sometimes even cell death. Yet given that 30,000 or more genes exist in the human genome and that the period from one human generation to another is about 30 years, one would expect as many as 10 or many more mutations in the passage of the genome from parent to child. As a further protection, however, each human genome is represented by two separate sets of chromosomes with almost identical genes. Therefore, one functional gene of each pair is almost always available to the child despite mutations. Most of the genes in the two chromosomes of each pair are identical or almost identical to each other, so it is usually stated that the different genes also exist in pairs, although occasionally this is not the case. Several nonhistone proteins are also major components of chromosomes, functioning both as chromosomal structural proteins and, in connection with the genetic regulatory machinery, as activators, inhibitors, and enzymes. The two newly formed chromosomes remain attached to each other (until time for mitosis) at a point called the centromere located near their center. The complex of microtubules extending between the two new centriole pairs is called the spindle, and the entire set of microtubules plus the two pairs of centrioles is called the mitotic apparatus. While the spindle is forming, the chromosomes of the nucleus (which in interphase consist of loosely coiled strands) become condensed into well-defined chromosomes. At the same time, multiple microtubules from the aster attach to the chromatids at the centromeres, where the paired chromatids are still bound to each other; the tubules then pull one chromatid of each pair toward one cellular pole and its partner toward the opposite pole. This pushing is believed to occur because the microtubular spines from the two asters, where they interdigitate with each other to form the mitotic spindle, actually push each other away. Minute contractile protein molecules called "molecular motors, which are perhaps " composed of the muscle protein actin, extend between the respective spines and, using a stepping action as in muscle, actively slide the spines in a reverse direction along each other. Simultaneously, the chromatids are pulled tightly by their attached microtubules to the very center of the cell, lining up to form the equatorial plate of the mitotic spindle. All 46 pairs of chromatids are separated, forming two separate sets of 46 daughter chromosomes. One of these sets is pulled toward one mitotic aster and the other is pulled toward the other aster as the two respective poles of the dividing cell are pushed still farther apart. Then the mitotic apparatus dissolutes, and a new nuclear membrane develops around each set of chromosomes. This membrane is formed from portions of the endoplasmic reticulum that are already present in the cytoplasm. This pinching is caused by formation of a contractile ring of microfilaments composed of actin and probably myosin (the two contractile proteins of muscle) at the juncture of the newly developing cells that pinches them off from each other. Once each chromosome has been replicated to form the two chromatids, in many cells, mitosis follows automatically within 1 or 2 hours. One of the first events of mitosis takes place in the cytoplasm; it occurs during the latter part of interphase in or around the small structures called centrioles. Each pair of centrioles, along with attached pericentriolar material, is called a centrosome. Shortly before mitosis is to take place, the two pairs of centrioles begin to move apart from each other. This movement is caused by polymerization of protein microtubules growing between the respective centriole pairs and actually pushing them apart. At the same time, other microtubules grow radially away from each of the centriole pairs, forming a spiny star, called the aster, in each end of the cell. Many other cells, however, such as smooth muscle cells, may not reproduce for many years. A few cells, such as the neurons and most striated muscle cells, do not reproduce during the entire life of a person, except during the original period of fetal life. In certain tissues, an insufficiency of some types of cells causes them to grow and reproduce rapidly until appropriate numbers of these cells are again available. For instance, in some young animals, seven eighths of the liver can be removed surgically, and the cells of the remaining one eighth will grow and divide until the liver mass returns to almost normal. The same phenomenon occurs for many glandular cells and most cells of the bone marrow, subcutaneous tissue, intestinal epithelium, and almost any other tissue except highly differentiated cells such as nerve and muscle cells. The mechanisms that maintain proper numbers of the different types of cells in the body are still poorly understood. However, experiments have shown at least three ways in which growth can be controlled. First, growth often is controlled by growth factors that come from other parts of the body. Some of these growth factors circulate in the blood, but others originate in adjacent tissues. For instance, the epithelial cells of some glands, such as the pancreas, fail to grow without a growth factor from the underlying connective tissue of the gland.

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In lead I ayurvedic treatment erectile dysfunction kerala erectafil 20 mg order, the recorded voltage of the injury poten tial is above the zero potential level and is therefore posi tive. In this instance, the resultant vector extends from the right side of the ventricles toward the left and slightly upward, with an axis of about -30 degrees. If one places this vector for the injury potential directly over the ventricles, the negative end of the vector points toward the permanently depolarized, "injured" area of the ventricles. Consequently, repo larization of the muscle membrane cannot occur in areas of severe myocardial ischemia. Often the heart muscle does not die because the blood flow is sufficient to main tain life of the muscle even though it is not sufficient to cause normal repolarization of the membranes. In other words, the negative end of the injury poten tial vector in this heart is against the anterior chest wall. This means that the current of injury is emanating from the anterior wall of the ventricles, which diagnoses this condition as anterior wall infarction. This finding means that the resultant vector of the injury potential in the heart is about +150 degrees, with the negative end pointing toward the left ventricle and the positive end pointing toward the right ventricle. Therefore, one would conclude that this anterior wall infarction almost certainly is caused by thrombosis of the anterior descending branch of the left coronary artery. By vectorial analysis, as shown in the figure, one finds that the resultant vector of the injury potential is about -95 degrees, with the nega tive end pointing downward and the positive end pointing upward. With use of the same procedures demonstrated in the preceding discussions of anterior and posterior wall infarctions, it is possible to determine the locus of any infarcted area emitting a current of injury, regardless of which part of the heart is involved. In making such vectorial analy ses, it should be remembered that the positive end of the injury potential vector points toward the normal cardiac muscle, and the negative end points toward the injured portion of the heart that is emitting the current of injury. This means that the positive end of the vector is in the direction of the anterior chest wall, and the negative end (the injured end of the vector) points away from the chest wall. However, after about 1 week, the injury potential has diminished considerably, and after 3 weeks, it is gone. This is the usual recovery pattern after acute myocardial infarction of moderate degree, showing that the new collateral coronary blood flow develops enough to reestablish appropriate nutrition to most of the infarcted area. In some patients who experience myocardial infarc tion, the infarcted area never redevelops adequate coro nary blood supply. Often, some of the heart muscle dies, but if the muscle does not die, it will continue to show an injury potential as long as the ischemia exists, particularly during bouts of exercise when the heart is overloaded. That is, the T wave becomes abnormal when the normal sequence of repolarization does not occur. The reason for this prolongation is delayed conduction in the left ventricle resulting from left bundle branch block. However, the refrac tory periods of the right and left ventricular muscle masses are not greatly different from each other. Therefore, the right ventricle begins to repolarize long before the left ventricle, which causes strong positivity in the right ven tricle and negativity in the left ventricle at the time that the T wave is developing. These configurations are certainly not found in all cases of old cardiac infarction. Usually, no pain is felt as long as the person is quiet, but as soon as he or she overworks the heart, the pain appears. Instead, the base of the ventricles would repolarize ahead of the apex, and the vector of repolarization would point from the apex toward the base of the heart, opposite to the standard vector of repolarization. Consequently, the T wave in all three standard leads would be negative rather than the usual positive. When the ischemia occurs in only one area of the heart, the depolarization period of this area decreases out of proportion to that in other portions. The ischemia might result from chronic, progressive cor onary occlusion, acute coronary occlusion, or relative coronary insufficiency that occurs during exercise. The changes in the T waves need not be specific because any change in the T wave in any lead-inversion, for instance, or a biphasic wave-is often evidence enough that some portion of the ventricular muscle has a period of depolar ization out of proportion to the rest of the heart, caused by mild to moderate coronary insufficiency. As discussed in Chapter 22, digitalis is a drug that can be used during coronary insufficiency to increase the strength of cardiac muscle contraction. As a result, nonspecific changes, such as Twave inversion or biphasic T waves, may occur in one or more of the electrocardiographic leads. Therefore, changes in the T wave during digitalis administration are often the earliest signs of digitalis toxicity. For instance, sometimes the beat of the atria is not coordinated with the beat of the ventricles, so the atria no longer function as primer pumps for the ventricles. The purpose of this chapter is to discuss the physiology of common cardiac arrhythmias and their effects on heart pumping, as well as their diagnosis by electrocardiography. Many factors can cause the sympathetic nervous system to excite the heart, as we discuss at multiple points in this text. For instance, when a patient sustains severe blood loss, sympathetic reflex stimulation of the heart may increase the heart rate to 150 to 180 beats/min. Simple weakening of the myocardium usually increases the heart rate because the weakened heart does not pump blood into the arterial tree to a normal extent, and this phenomenon causes reductions in blood pressure and elicits sympathetic reflexes to increase the heart rate. Some causes of tachycardia include increased body temperature, stimulation of the heart by the sympathetic nerves, or toxic conditions of the heart. When the athlete is at rest, excessive quantities of blood pumped into the arterial tree with each beat initiate feedback circulatory reflexes or other effects to cause bradycardia.

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The veins function as conduits for transport of blood from the venules back to the heart; equally important what std causes erectile dysfunction purchase erectafil cheap, they serve as a major reservoir of extra blood. Even so, they are muscular enough to contract or expand and thereby serve as a controllable reservoir for the extra blood, either a small or a large amount, depending on the needs of the circulation. Because the systemic circulation supplies blood flow to all the tissues of the body except the lungs, it is also called the greater circulation or peripheral circulation. Before discussing the details of circulatory function, it is important to understand the role of each part of the circulation. The function of the arteries is to transport blood under high pressure to the tissues. For this reason, the arteries have strong vascular walls, and blood flows at a high velocity in the arteries. The arterioles are the last small branches of the arterial system; they act as control conduits through which blood is released into the capillaries. Arterioles have strong lation and lists the percentage of the total blood volume in major segments of the circulation. For instance, about 84 percent of the entire blood volume of the body is in the systemic circulation and 16 percent is in the heart and lungs. Of the 84 percent in the systemic circulation, approximately 64 percent is in the veins, 13 percent is in the arteries, and 7 percent is in the systemic arterioles and capillaries. It is here, however, that the most important function of the circulation occurs-diffusion of substances back and forth between the blood and the tissues. Vessel Aorta Smallarteries Arterioles Capillaries Venules Smallveins Venaecavae Cross-Sectional Area (cm2) 2. As the blood flows through the systemic circulation, its mean pressure falls progressively to about 0 mm Hg by the time it reaches the termination of the superior and inferior venae cavae where they empty into the right atrium of the heart. The pressure in the systemic capillaries varies from as high as 35 mm Hg near the arteriolar ends to as low as 10 mm Hg near the venous ends, but their average "functional" pressure in most vascular beds is about 17 mm Hg, a pressure low enough that little of the plasma leaks through the minute pores of the capillary walls, even though nutrients can diffuse easily through these same pores to the outlying tissue cells. In the pulmonary arteries, the pressure is pulsatile, just as in the aorta, but the pressure is far less: pulmonary artery systolic pressure averages about 25 mm Hg and diastolic pressure averages about 8 mm Hg, with a mean pulmonary arterial pressure of only 16 mm Hg. Yet, the total blood flow through the lungs each minute is the same as through the systemic circulation. The low pressures of the pulmonary system are in accord with the needs of the lungs because all that is required is to expose the blood in the pulmonary capillaries to oxygen and other gases in the pulmonary alveoli. Because the heart pumps blood continually into the Note particularly that the cross-sectional areas of the veins are much larger than those of the arteries, averaging about four times those of the corresponding arteries. This difference explains the large blood storage capacity of the venous system in comparison with the arterial system. When tissues are active, they need a greatly increased supply of nutrients and therefore much more blood flow than when at rest- occasionally as much as 20 to 30 times the resting level. Yet, the heart normally cannot increase its cardiac output more than four to seven times greater than resting levels. Therefore, it is not possible simply to increase blood flow everywhere in the body when a particular tissue demands increased flow. Instead, the microvessels of each Thus, under resting conditions, the velocity averages about 33 cm/sec in the aorta but is only 1/1000 as rapid in the capillaries-about 0. Also, nervous control of the circulation from the central nervous system and hormones provide additional help in controlling tissue blood flow. When blood flows through a tissue, it immediately returns by way of the veins to the heart. The heart responds automatically to this increased inflow of blood by pumping it immediately back into the arteries. The heart, however, often needs help in the form of special nerve signals to make it pump the required amounts of blood flow. Arterial pressure regulation is generally independent of either local blood flow control or cardiac output control. The circulatory system is provided with an extensive system for controlling the arterial blood pressure. For instance, if at any time the pressure falls significantly below the normal level of about 100 mm Hg, within seconds a barrage of nervous reflexes elicits a series of circulatory changes to raise the pressure back toward normal. The nervous signals especially (a) increase the force of heart pumping, (b) cause contraction of the large venous reservoirs to provide more blood to the heart, and (c) cause generalized constriction of the arterioles in many tissues so that more blood accumulates in the large arteries to increase the arterial pressure. Then, over more prolonged periods- hours and days-the kidneys play an additional major role in pressure control both by secreting pressure-controlling hormones and by regulating the blood volume. Thus, the needs of the individual tissues are served specifically by the circulation. In the remainder of this chapter, we begin to discuss the basic details of the management of tissue blood flow and control of cardiac output and arterial pressure. P1 represents the pressure at the origin of the vessel; at the other end, the pressure is P2. Resistance occurs as a result of friction between the flowing blood and the intravascular endothelium all along the inside of the vessel. This formula states that the blood flow is directly proportional to the pressure difference but inversely proportional to the resistance. Note that it is the difference in pressure between the two ends of the vessel, not the absolute pressure in the vessel, that determines rate of flow. For example, if the pressure at both ends of a vessel is 100 mm Hg and yet no difference exists between the two ends, there will be no flow despite the presence of 100 mm Hg pressure.

Givess, 36 years: Below it is continuous with a wide shallow groove, bounded laterally by the anterior inferior iliac spine and medially by the iliopubic ramus. Blood escapes from the superficial vessels of the endometrium, forming small haematomata beneath the surface epithelium (see below). Within a few seconds, a new circulatory state is established at point B, illustrating that the cardiac output has fallen to 2 L/min, about two-fifths normal, whereas the right atrial pressure has risen to +4 mm Hg because venous blood returning to the heart from the body is dammed up in the falls precariously low, many of the circulatory reflexes discussed in Chapter 18 are rapidly activated. Medial or lateral gastrocnemius musculocutaneous flaps may be raised, each based on its neurovascular pedicle.

Sanuyem, 58 years: We explain later in the chapter that the cardiac output is regulated throughout life almost directly in proportion to overall metabolic activity. During these 5 to 20 seconds, the ventricles fail to pump blood, and the person faints after the first 4 to 5 seconds because of lack of blood flow to the brain. Key: 1, long saphenous vein and saphenous nerve; 2, medial malleolus; 3, lateral malleolus; 4, dorsalis pedis artery and deep fibular nerve: located immediately lateral to the tendon of extensor hallucis longus; 5, intermediate dorsal cutaneous nerve: visible passing towards the fourth digit during digit and ankle plantar flexion; 6, extensor digitorum brevis; 7, tendon of extensor hallucis longus; 8, tendon of tibialis anterior: insertion into medial cuneiform; 9, tuberosity of fifth metatarsal; 10, dorsal venous arch of foot; 11, tendon of extensor digitorum longus (to digit two). Study of smooth muscle progenitors shows that the bulk of the trigone derives from bladder muscle (detru sor), with a limited contribution from ureteral longitudinal smooth muscle fibres at the lateral edges.

Kadok, 51 years: Cardiotonic 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. Levator ani must relax appropriately to permit expulsion of urine and, particularly, faeces; it contracts with the abdominal muscles and the abdominothoracic diaphragm to raise intra-abdominal pressure. Lower in the thigh, arterial branches derived from the perforating branches of the profunda femoris artery or the anastomotic chain between them or, occasionally, from the popliteal artery, enter the nerve on its lateral or anterolateral side (Sunderland 1945). The verumontanum is used as a surgical landmark for the urethral sphincter during transurethral resection for benign enlargement of the prostate.

Mason, 48 years: Key: 1, gap in capsule for popliteus tendon; 2, soleus; 3, flexor 10 hallucis longus; 4, fibularis brevis; 5, epiphysial line (growth plate); 6, capsular attachment; 7, semimembranosus; 8, epiphysial lines (growth plates); 9, popliteus; 10, soleus; 11, tibialis posterior; 12, flexor digitorum longus; 13, epiphysial line (growth plate); 14, capsular attachment. It is believed that much of this adenosine leaks out of the heart muscle cells to cause coronary vasodilation, providing increased coronary blood flow to supply the increased nutrient demands of the active heart. The patella is a sesamoid bone in the quadriceps femoris tendon, and the patellar ligament, which extends from the patellar apex to the tibial tuberosity, is the continuation of the main tendon. Disorders of development of the testis and reproductive tract in the male fetus seem to be increasing in incidence.

Brontobb, 45 years: In infancy, dimensions of the whole pelvis are greater in males than in females, but the size of the pelvic cavity is usually greater in females. The impaired locking mechanism diverts the strain of weight-bearing to the ligaments, with frequent sacroiliac strain after pregnancy. The kidneys, for instance, often entirely cease their production of urine because of renal arteriolar constric tion in response to the sympathetic discharge. The artery to the bulb supplies the corpus spongiosum, and the cavernous artery of the penis supplies the corpus cavernosum on each side.