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Venous occlusion plethysmography is a simple but elegant technique that has contributed to almost every major area of vascular biology in humans. The general principles of plethysmography were appreciated by the late 1800s, and the application of these principles to measure limb blood flow occurred in the early 1900s. Plethysmography has been instrumental in studying the role of the autonomic nervous system in regulating limb blood flow in humans and important in studying the vasodilator responses to exercise, reactive hyperemia, body heating, and mental stress. It has also been the technique of choice to study how human blood vessels respond to a variety of exogenously administered vasodilators and vasoconstrictors, especially those that act on various autonomic and adrenergic receptors. In recent years, plethysmography has been exploited to study the role of the vascular endothelium in health and disease. Venous occlusion plethysmography is likely to continue to play an important role as investigators seek to understand the physiological significance of newly identified vasoactive factors and how genetic polymorphisms affect the cardiovascular system in humans.

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OBJECTIVE: This study investigated one aspect of the role of school-based occupational therapists working with students with complex health care needs during the school day. METHOD: One hundred seventy-two occupational therapists working in school systems were surveyed with regard to their involvement with children with complex health care needs, particularly specific complex health care procedures performed, knowledge of policies, training in the administration of health-related procedures, and perceived levels of competency. RESULTS: Sixty-eight (61%) of the therapists reported having children with complex health care needs on their caseload; of these, 65% reported involvement in seizure monitoring and 24% reported performing gastrostomy feedings. Most respondents reported an awareness of policies regarding administration of medication, gastrostomy feeding, and seizure monitoring in their school system. Respondents' main role with this population included activities in positioning, environmental modification, and staff instruction. CONCLUSION: The major role of occupational therapists working in school systems involved providing direct intervention with the student and not conducting or instructing others in health-related procedures. Therapists also served as a resource on health-related issues for school personnel.

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Professor Henry Barcroft, MD, FRS, Emeritus Professor of Physiology in St. Thomas' Hospital Medical School in London died on 11 January 1998, aged 93. He was born in Cambridge on 18 October 1904 where his father, Joseph Barcroft, a famous physiologist, worked with Foster and Langley and subsequently was appointed to the Chair of Physiology. Henry Barcroft followed in his father's footsteps. During his career as Professor of Physiology firstly at The Queen's University of Belfast and subsequently at St. Thomas's Hospital London, he made significant studies on the nervous and humoral control of human blood vessels. His success as a research scientist stemmed partly from his ability to simplify complex phenomena in a way that permitted them to be broken into component parts and tested and partly from his technical ingenuity that permitted simple, inexpensive measurements of difficult physiological variables. Perhaps the most important factor, however, was his ability to bring out and stimulate aptitudes and enthusiasms in others. Completely unselfish himself, he gave individuals every opportunity to develop their talents, and so make themselves known to a wide circle of interested medical scientists. In many ways, his life was a guidebook for young scientists on how to make the most of their opportunities.

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During vasovagal syncope, profound bradycardia and hypotension occur. Atropine administration can prevent the bradycardia but not the hypotension, suggesting that marked peripheral vasodilation is a major cause of the fall in arterial pressure. This concept has been confirmed since vasovagal syncope can be seen in patients who have undergone heart transplantation and also in patients subject to cardiac pacing. In both cases, there is no bradycardia but hypotension during the syncopal attacks. The major site of the vasodilation is in skeletal muscle and muscle sympathetic nerve activity is suppressed just prior to and during vasovagal attacks, indicating that sympathetic withdrawal contributes to the dilation. However, the skeletal muscle vasodilation seen during syncope is greater than that caused by sympathetic withdrawal alone, and it is absent in limbs that have undergone surgical sympathectomy, or local anesthetic nerve block. These observations suggest a role for neurally mediated "active" vasodilation during syncope. The afferent neural pathways that evoke the profound vasodilation during vasovagal attacks remain the subject of debate. The neural pathways responsible for the active component of the dilation are also unknown. Recent evidence has demonstrated that cholinergic, beta-adrenergic, and nitroxidergic (nitric oxide) vasodilator mechanisms are not essential to observe the dilation, demonstrating that the mechanisms responsible for it remain a continuing conundrum.

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Gravitational stresses, which are common daily event for humans, result in a diminution in central blood volume, due to displacement of blood to the lower parts of the body. They demand complex adjustments in the cardiovascular system to offset the decrease in cardiac filling pressure. Such changes are necessary to sustain arterial blood pressure at an appropriate level so that there is adequate perfusion of vital organs, especially the brain. These adjustments must compensate for both the initial and sustained orthostatic stress. The rapid short-term adaptations are mediated primarily by the cardiovascular reflexes with humoral agents reinforcing these reflexes during severe and prolonged orthostatic stress. Understanding these complex reflex adjustments in normal humans is necessary in order to appreciate subjects with orthostatic intolerance.

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Much has been learned about the complexity of the local, humoral and nervous factors regulating the normal behavior of the skin blood vessels, and many studies have addressed how this knowledge might relate to the causation of primary Raynaud's disease. Despite this, the mechanism(s) responsible for the attacks of digital vasospasm remain an enigma. A key question is whether these attacks represent an exaggeration of the normal mechanisms causing constriction of the digital vessels with local cooling, or are due to a specific abnormality. In this article it is suggested that multiple factors are responsible, including the possibility of co-transmitters released with norepinephrine from the sympathetic nerves, increased activation of beta 2-adrenoceptors on the nerve endings, a shift in the balance of alpha 1 and alpha 2 adrenoceptors on the vascular smooth muscle and in endothelium-derived relaxing and contracting factors, and altered interactions of the endothelium with the blood elements including the effects of increased platelet serotonin.

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Evidence continues to accumulate on the importance of paracrine substances formed in the vascular endothelium in the regulation of the vascular system. Those that relax the underlying smooth muscle include nitric oxide, prostacyclin, and an unidentified hyperpolarizing factor; those causing contraction include angiotensin II, endothelin, oxygen-derived free radicals, prostacyclin H2, and thromboxane A2. Determination of the mechanisms governing the formation and release of these substances in different blood vessels of the same species and in different species as well as the maintenance of the balance between them is important for understanding their role in normal circumstances and in diseases of the blood vessels. In this article, we will summarize the current understanding of the role of endothelium-derived relaxing factors and discuss the possibility that endothelial dysfunction may play a primary as well as a secondary role in the pathogenesis of primary hypertension. As a consequence of this dysfunction, substances formed in the endothelial cells at the sites of the arterial baroreceptors could lead to their resetting, resulting in less inhibition of the vasomotor centers, enhanced neurohumoral activity, and a consequential increase in systemic vascular resistance. This increase could be enhanced by a predominant action of endothelium-derived contracting factors in the resistance vessels. Proliferation of the vascular smooth muscle would follow, because of the mitogenic action of some of these factors and other growth promotors. By these mechanisms, the endothelium may participate in the polygenic dysfunction characteristic of primary hypertension, not only in initiating the increase in arterial blood pressure, but also in sustaining it.

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Endothelial cells may produce and release vasoconstrictor substances in response to a number of agents and physical stimuli. In this brief review, current understanding of the mechanisms of endothelium-dependent contractions will be discussed. Cyclooxygenase products of arachidonic acid metabolism including thromboxane A2, prostaglandin H2, superoxide anions, vasoconstrictor peptide endothelin-1, and unidentified factor released from endothelium by hypoxia may mediate these contractions. The physiological role of endothelium-dependent contractions in regulation of the cardiovascular system is unknown. Existing evidence supports the concept that contracting factors may become important regulators of vascular tone under pathological conditions. We speculated about the possible importance of endothelium-dependent contractions for venous graft function, development of vasospasm, increased vascular resistance in hypertension, and vascular complications in diabetes.

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Studies in recent years have demonstrated that coronary vasospasm (Prinzmetal's Angina) is a consequence of endothelial cell damage. Normal endothelium, in response to increases in shear stress, or to platelet products and other agonists, releases endothelium-derived relaxing factor(s) (EDRF) with resultant vasodilatation. One substance released may be nitric oxide, another a hyperpolarizing factor. In addition EDRF like prostacyclin, inhibits platelet aggregation. In porcine coronary vessels the amount of EDRF released can be increased by a diet of codliver oil and decreased by a high cholesterol diet. When endothelium is damaged, the absence of EDRF and prostacyclin at the site leads to platelet aggregation with the release, among other substances, of serotonin (5HT) and thromboxane A2. These now act directly on the smooth muscle to cause contraction. In addition some serotonin is taken up by the sympathetic nerve endings and is released as a false transmitter to aggravate the constriction. The resultant hypoxia/anoxia can cause any functional endothelium to release contracting factor(s), further compounding the constriction. Evidence of platelet aggregation in humans is the presence of serotonin in the coronary sinus blood in resting patients with coronary artery disease.

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Polygenetic predisposition is a key factor in the multifactorial disorders of primary hypertension. It is suggested that endothelial cell abnormalities are the major factors responsible for the increase in total systemic vascular resistance that leads to an elevation in arterial blood pressure. Thus, resetting of the arterial baroreceptors could be a consequence of endothelial-mediated changes in mechano-electrical transduction in the arterial mechanoreceptors. In consequence, inhibition of the vasomotor centers would be diminished and the resulting neurohumoral excitation would constrict the systemic resistance blood vessels. Later, as left ventricular hypertrophy develops, the inhibitory input of the cardiac mechanoreceptors is also reduced. In normal endothelial cells there is a predominant formation and release of vascular smooth muscle relaxing and growth-inhibiting factors. However, it is proposed that genetic changes lead to a predominate formation of endothelium-derived contracting factors and mitogens. The former would augment the neurohumoral vasoconstriction. The latter, aided by the increased arterial pressure and the augmented output of norepinephrine, would lead to structural alterations in the arterial vessels, thus reducing the lumen area, amplifying the vasoconstrictor response to contractile agents and limiting vasodilation. In this way the hypertension would be perpetuated.

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Women are far more likely than men to suffer from Raynaud's disease. The purpose of this study was to determine whether there are gender differences in local or central control of cutaneous blood flow that could account for the increased incidence of Raynaud's disease in women. To assess cutaneous blood flow, hand blood flow (HBF), finger blood flow (FBF), or skin perfusion (SP) was measured by fluid plethysmography, mercury strain-gauge plethysmography, or laser Doppler spectroscopy, respectively, in 47 volunteers. Basal HBF in men exceeded that of women (12.1 +/- 2.0 versus 6.2 +/- 1.5 ml/100 ml/min). Likewise, FBF in men surpassed that of women (19.5 +/- 4.1 versus 7.7 +/- 1.8 ml/100 ml/min). Similarly, SP in men was greater than that of women (270 +/- 42 versus 81 +/- 16 perfusion units). However, after total body warming (to induce a thermal sympatholysis), HBF in women exceeded that of men, suggesting that the lower basal HBF in women was due to increased sympathetic outflow to the extremities. Mental stress and deep inspiration reduced HBF and SP in men. Paradoxically, both of these maneuvers increased HBF and SP in women. To determine whether these paradoxical responses in women were due to the women's elevated basal sympathetic tone, these experiments were repeated after total body cooling in men to increase sympathetic tone and after total body warming in women to reduce sympathetic tone. Total body cooling reduced HBF and SP in men. Under these conditions, mental stress and deep inspiration induced vasodilation. In women, total body warming for 10 minutes increased HBF.(ABSTRACT TRUNCATED AT 250 WORDS)

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The purpose of this study was to examine the effects of the increased sympathetic activity elicited by the upright posture on blood flow to exercising human forearm muscles. Six subjects performed light and heavy rhythmic forearm exercise. Trials were conducted with the subjects supine and standing. Forearm blood flow (FBF, plethysmography) and skin blood flow (laser Doppler) were measured during brief pauses in the contractions. Arterial blood pressure and heart rate were also measured. During the first 6 min of light exercise, blood flow was similar in the supine and standing positions (approximately 15 ml.min-1.100 ml-1); from minutes 7 to 20 FBF was approximately 3-7 ml.min-1.100 ml-1 less in the standing position (P less than 0.05). When 5 min of heavy exercise immediately followed the light exercise, FBF was approximately 30-35 ml.min-1.100 ml-1 in the supine position. These values were approximately 8-12 ml.min-1.100 ml-1 greater than those observed in the upright position (P less than 0.05). When light exercise did not precede 8 min of heavy exercise, the blood flow at the end of minute 1 was similar in the supine and standing positions but was approximately 6-9 ml.min-1.100 ml-1 lower in the standing position during minutes 2-8. Heart rate was always approximately 10-20 beats higher in the upright position (P less than 0.05). Forearm skin blood flow and mean arterial pressure were similar in the two positions, indicating that the changes in FBF resulted from differences in the caliber of the resistance vessels in the forearm muscles.(ABSTRACT TRUNCATED AT 250 WORDS)

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The purpose of this study was to determine whether prolonged unloading of cardiopulmonary baroreceptors with lower body negative pressure (LBNP) causes constant increases in sympathetic outflow to skeletal muscles. Eight healthy subjects underwent a 20-min control period followed by 20 min of 15-mmHg LBNP. This pressure was selected because it did not cause any significant change in mean arterial blood pressure (sphygmomanometry) or heart rate, suggesting that the cardiopulmonary baroreceptors were selectively unloaded and the activity of the arterial baroreceptors was unchanged. Muscle sympathetic nerve activity in the peroneal nerve (MSNA, microneurography) increased from an average of 21.8 +/- 1.7 bursts/min over the last 5 min of control to 29.0 +/- 2.9 bursts/min during the 1st min of LBNP (P less than 0.05 LBNP vs. control). The increase in MSNA observed during the 1st min was sustained throughout LBNP. Forelimb blood flow (plethysmography) decreased abruptly at the onset of the LBNP from a control value of 4.3 +/- 0.5 ml.min-1.100 ml-1 to 2.5 +/- 0.2 at the 1st min; the flow then increased and remained significantly above this value, but below the control value, throughout LBNP. Similar blood flow findings were obtained in additional studies, when the hand circulation was excluded during the flow measurements. Forearm skin blood flow (laser Doppler) also decreased abruptly at the onset of LBNP and was followed by partial recovery, but these changes were too small to account for all the increases in limb blood flow over the course of LBNP.(ABSTRACT TRUNCATED AT 250 WORDS)

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The cardiovascular reflexes have the key role in the rapid adjustments of the circulatory system in response to daily stresses such as standing and muscular exercise. Arterial and cardiopulmonary mechanoreceptors continuously signal to the cardiovascular centers in the brain the moment to moment pressure changes in the larger arteries, atria and ventricles and exert a tonic restraint on the sympathetic noradrenergic outflow. Depending on the stress, the vasomotor centers adjust this outflow, both qualitatively and quantitatively, to the heart and to the different vascular beds to maintain an appropriate arterial blood pressure. In addition, the sympathetic nerves modulate renin release from the juxtaglomerular cells and receptors at the veno-atrial junctions regulate vasopressin release from the posterior pituitary. Congestive heart failure is characterized by excessive neuro-humoral excitation as evidenced by direct recordings of sympathetic activity and by increased plasma levels of catecholamines, renin, angiotensin II and arginine vasopressin. The evidence indicates that this is a consequence of the reduced ability of the arterial and cardiopulmonary mechanoreceptors to inhibit the vasomotor centers. The cause(s) of this diminished circulatory control requires further studies. The cardiac glycosides, which normally cause vasoconstriction, cause vasodilatation in patients with heart failure. This is attributed to sensitization of the mechanoreceptors. The term atrial natriuretic factor refers to a family of peptide hormones released when the atrial myocytes are stimulated by an increase in transmural pressure. They cause diuresis, natriuresis and vasorelaxation. In severe congestive heart failure, the plasma levels are increased and this helps to compensate for the increased neurohumoral activation by inhibiting the renin-angiotensin system and enhancing sodium and water excretion.(ABSTRACT TRUNCATED AT 250 WORDS)

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