透析低血压与非透析低血压血容量状况的分析

目的分析血液透析和超滤过程中透析相关低血压的发生与血容量变化的关系.探讨症状性透析低血压的防治策略.方法以过去3月内发生过症状性透析低血压为观测组(23例),设无透析低血压的为对照组(28例).应用超声血容量检测仪比较透析低血压者和正常对照者在透析超滤过程中血容量的变化特点、以及血压、心率的相应变化.结果低血压组的透析间体重增加量、超滤量明显高于对照组(P＜0.02).透析1小时后相对血容量、血压的下降程度超过对照组(P＜0.05);而反射性的心率增快方面,低血压组低于对照组(P＜0.05).结论血容量下降是发生低血压的重要机制,尤其是透析者伴有心血管功能损害时,更易发生透析低血压.而提高血容量是治疗症状性透析低血压的关键措施.     

Adrenergic regulation of blood pressure in chronic renal failure.

Previous investigations have suggested that significant hypotension during hemodialysis may result from abnormalities of sympathetic nervous system activity. To further evaluate these phenomena, plasma dopamine beta-hydroxylase (D beta H) and cold pressor test (proposed indexes of efferent sympathetic nervous system activity) and amyl nitrite inhalation (an index of the entire baroreceptor reflex arc) were studied in two groups of patients: group I, patients exhibiting a mean arterial pressure decrease to less than 70 mm Hg during less than 10% of dialyses; group II (hemodialysis hypotension), patients with a mean arterial pressure decrease to less than 70 mm Hg during more than 90% of dialyses. The groups were similar with respect to plasma renin activity, renin response to ultrafiltration, age, duration of dialysis, nerve conduction velocity, plasma protein concentration, hematocrit, dialysis weight change, resting heart rate, sex, race, blood pressure and heart rate response to cold pressor test, and 125I-albumin plasma volume. Supine mean arterial pressure was higher in patients with hemodialysis hypotension than in patients without hemodialysis hypotension (group I) both before and after dialysis. Plasma D beta H activity was significantly higher in patients with hemodialysis hypotension (group II) than in group I both before and after dialysis. Amyl nitrite inhalation, expressed as change in delta R-R interval/mean arterial pressure decrease, was less in hemodialysis hypotension patients. These results suggest that hemodialysis hypotension may result from a lesion in the baroreceptors, cardiopulmonary receptors, or visceral afferent nerves. Furthermore, elevated mean arterial pressure in patients with hemodialysis hypotension may be neurogenic in origin, as reflected by plasma D beta H activity, and appears similar to the hypertension that follows baroreceptor deafferentation of experimental animals.     

Contrasting neurovascular findings in chronic orthostatic intolerance and neurocardiogenic syncope

Simple faint (neurocardiogenic syncope) and postural tachycardia syndrome (POTS) characterize acute and chronic orthostatic intolerance respectively. We explored the hypothesis that vascular function is similar in the two conditions. We studied 29 patients with POTS and compared them with 20 patients with neurocardiogenic syncope who were otherwise well, and with 15 healthy control subjects. We measured continuous heart rate, respiration and blood pressure, and used venous occlusion strain gauge plethysmography to measure calf and forearm blood flow, peripheral arterial resistance, peripheral venous resistance and venous pressure ( P (v)). Upright tilt was performed to 70 degrees for 10 min, during which calf blood flow and volume were measured. Calf P (v) was increased (to 27.2+/-2.0 mmHg) in a subgroup of POTS patients, who also had increased arterial resistance (57+/-6 mmHg.ml(-1).min(-1).100 ml(-1) tissue), increased venous resistance (2.4+/-0.3 mmHg.ml(-1).min(-1).100 ml(-1) tissue), and decreased peripheral flow (1.0+/-0.2 ml.min(-1).100 ml(-1) tissue) in the calf; other POTS patients with a normal P (v) had decreased arterial resistance (18+/-2 mmHg.ml(-1).min(-1).100 ml(-1) tissue) and increased blood flow (3.8+/-0.3 ml.min(-1).100 ml(-1) tissue). Syncope patients were not different from controls ( P (v)=11.4+/-0.5 mmHg; calf flow=3.1+/-0.2 ml.min(-1).100 ml(-1) tissue; arterial resistance=27+/-2 mmHg.ml(-1).min(-1).100 ml(-1) tissue; venous resistance=1.2+/-0.3 mmHg.ml(-1).min(-1).100 ml(-1) tissue). When upright, syncope patients and control subjects had similar increases in heart rate and calf volume, stable blood pressure, and decreases in blood flow. POTS patients had markedly increased heart rate and calf blood flow, unstable blood pressure, and pooling in the lower extremities, regardless of subgroup. We conclude that peripheral vascular physiology in patients with POTS is abnormal, in contrast with normal peripheral vascular physiology in neurocardiogenic syncope.     

Sympathetic and baroreceptor reflex function in neurally mediated syncope evoked by tilt.

The pathophysiology of neurally mediated syncope is poorly understood. It has been widely assumed that excessive sympathetic activation in a setting of left ventricular hypovolemia stimulates ventricular afferents that trigger hypotension and bradycardia. We tested this hypothesis by determining if excessive sympathetic activation precedes development of neurally mediated syncope, and if this correlates with alterations in baroreflex function. We studied the changes in intraarterial blood pressure (BP), heart rate (HR), central venous pressure (CVP), muscle sympathetic nerve activity (MSNA), and plasma catecholamines evoked by upright tilt in recurrent neurally mediated syncope patients (SYN, 5+/-1 episodes/mo, n = 14), age- and sex-matched controls (CON, n = 23), and in healthy subjects who consistently experienced syncope during tilt (FS+, n = 20). Baroreflex responses were evaluated from changes in HR, BP, and MSNA that were obtained after infusions of phenylephrine and sodium nitroprusside. Compared to CON, patients with SYN had blunted increases in MSNA at low tilt levels, followed by a progressive decrease and ultimately complete disappearance of MSNA with syncope. SYN patients also had attenuation of norepinephrine increases and lower baroreflex slope sensitivity, both during tilt and after pharmacologic testing. FS+ subjects had the largest decrease in CVP with tilt and had significant increases in MSNA and heart rate baroreflex slopes. These data challenge the view that excessive generalized sympathetic activation is the precursor of the hemodynamic abnormality underlying recurrent neurally mediated syncope.     

Neurohumoral antecedents of vasodepressor reactions

Abstract. Vasodepressor (vasovagal) syncope, the most common cause of acute loss of consciousness, can occur in otherwise vigorously healthy people during exposure to stimuli decreasing cardiac filling. Antecedent physiological or neuroendocrine conditions for this dramatic syndrome are poorly understood. This study compared neurocirculatory responses to non-hypotensive lower body negative pressure (LBNP) in subjects who subsequently developed vasodepressor reactions during hypotensive LBNP with responses in subjects who did not. In 26 healthy subjects, LBNP at -15 and -40mmHg was applied to inhibit cardiopulmonary and arterial baroreceptors. All the subjects tolerated 30min of LBNP at -15 mmHg, but during subsequent LBNP at -40 mmHg 11 subjects had vasodepressor reactions, with sudden hypotension, nausea, and dizziness. In these subjects, arterial plasma adrenaline responses to LBNP both at -15 and at -40 mmHg exceeded those in subjects who did not experience these reactions. In 16 of the 26 subjects, forearm noradrenaline spillover was measured; in the eight subjects with a vasodepressor reaction, mean forearm noradrenaline spillover failed to increase during LBNP at -15mmHg (Δ= -0.06±(SEM) 0.04pmol min^-1 100mL^-1), whereas in the eight subjects without a vasodepressor reaction, mean forearm noradrenaline spillover increased significantly (Δ=0.31±0.13pmolmin^-1100mL^-1). Plasma levels of β-endorphin during LBNP at -15 mmHg increased in some subjects who subsequently had a vasodepressor reaction during LBNP at -40 mmHg. The findings suggest that a neuroendocrine pattern including adre-nomedullary stimulation, skeletal sympathoinhibition, and release of endogenous opioids can precede vasodepressor syncope.     

Water ingestion increases sympathetic vasoconstrictor discharge in normal human subjects

A marked pressor response to water drinking has been observed in patients with autonomic failure and in the elderly, and has been attributed to sympathetic vasoconstrictor activation, despite the absence of such a pressor response in healthy subjects with intact sympathetic mechanisms. We investigated whether water drinking in normal subjects affected peripheral sympathetic neural discharge and its effect on vascular resistance. In nine normal human subjects, we examined the effect of water ingestion on muscle sympathetic neural activity from the peroneal nerve, as multi-unit bursts (muscle sympathetic nerve activity; MSNA) and as single-unit impulses (s-MSNA) with vasoconstrictor function, and on calf vascular resistance for 120 min. In each subject, water ingestion caused increases in s-MSNA and MSNA which peaked at 30 min after ingestion; they increased respectively (mean+/-S.E.M.) from 42+/-4 to 58+/-5 impulses/100 beats (P<0.01) and from 36+/-4 to 51+/-5 bursts/100 beats (P<0.001). There were corresponding increases in calf vascular resistance and in plasma noradrenaline levels. A significant correlation occurred between all of these data. In conclusion, measurement of MSNA has provided direct evidence that water drinking in normal human subjects increases sympathetic nerve traffic, leading to peripheral vasoconstriction. This sympathetic activation was not accompanied by significant changes in arterial blood pressure.     

Sympathetic and hemodynamic adjustments to hemorrhage: a possible role for endogenous opioid peptides

The traditional view of the decrease in blood pressure during blood loss is that it is a passive phenomenon. Blood pressure falls due to the inability of the compensatory mechanisms to keep pace with blood loss. However, recent evidence indicates that this transition from normotension to hypotension may involve an active decrease in compensation by the sympathetic nervous system. In the conscious, chronically prepared rabbit, blood pressure is maintained early in hemorrhage primarily by sympathetically mediated compensatory increases in vascular resistance and heart rate. When blood loss exceeds approximately 20% of total blood volume, hypotension develops abruptly due to a decrease in vascular resistance. This vasodilation is accompanied by decreased plasma norepinephrine (NE) levels and decreased sympathetic nerve activity. Therefore, the transition from normotension to hypotension during hemorrhage involves an active change, a decrease in vascular resistance, associated with a decrease in sympathetic nerve activity. Opioid receptor blockade with naloxone reverses acute hemorrhagic hypotension by increasing vascular resistance. The increase in resistance is accompanied by increased plasma NE and increased sympathetic nerve activity. Thus, the transition to hypotension during acute hemorrhage may be an active event brought on by a decrease in sympathetic outflow. Naloxone's reversal of the hypotension is consistent with the central involvement of endogenous opioid peptides in this phenomenon and thus in the pathogenesis of hypotension during blood loss.     

Orthostatic challenge reveals impaired vascular resistance control,but normal venous pooling and capillary filtration in familial dysautonomia

Patients with familial dysautonomia (FD) frequently have profound orthostatic hypotension without compensatory tachycardia. Although the aetiology is presumed to be sympathetic impairment, peripheral vascular responses to orthostasis have not been assessed. The aim of this study was to evaluate the control of vascular responses to postural stress in FD patients. Measurements of heart rate, blood pressure, cardiac stroke volume and cardiac output (CO), by impedance cardiography, and calf-volume changes, by impedance plethysmography, were taken from nine FD patients and 11 control subjects while supine and during head-up tilt. During leg lowering, we also assessed the venoarteriolar reflex by measuring skin red-cell flux. Head-up tilting for 10 min induced sustained decreases in mean arterial pressure in the FD patients, but not in the controls. Total peripheral resistance (TPR, i.e. mean arterial pressure/CO) increased significantly in the controls (39.8+/-6.8%), but not in the FD patients. Calf-volume changes during tilting, when normalized for the initial calf volume, did not differ significantly between the patients (4.62+/-1.99 ml.100 ml(-1)) and the controls (3.18+/-0.74 ml.100 ml(-1)). The vasoconstrictor response to limb lowering was present in the patients (47.7+/-9.0% decrease in skin red-cell flux), but was impaired as compared with the controls (80.7+/-3.4%) ( P <0.05). The impaired vasoconstriction during limb lowering and absent increase of TPR during tilting confirm that orthostatic hypotension in FD is due primarily to a lack of sympathetically mediated vasoconstriction without evidence of abnormally large shifts in blood volume towards the legs during orthostasis. This may be due, in part, to a preserved myogenic response to increased vascular pressure in the dependent vascular beds.     

Autonomic control of the venous system in health and disease: effects of drugs

The venous system contains 70% of the blood volume. The sympathetic nervous system is by far the most important vasopressor system in the control of venous capacitance. The baroreflex system responds to acute hypotension by concurrently increasing sympathetic tone to resistance, as well as capacitance vessels, to increase blood pressure and venous return, respectively. Studies in experimental animals have shown that interference of sympathetic activity by an ₁- or ₂-adrenoceptor antagonist or a ganglionic blocker reduces mean circulatory filling pressure and venous resistance and increases unstressed volume. An ₁- or ₂-adrenoceptor agonist, on the other hand, increases mean circulatory filling pressure and venous resistance and reduces unstressed volume. In humans, drugs that interfere with sympathetic tone can cause the pooling of blood in limb as well as splanchnic veins; the reduction of cardiac output; and orthostatic intolerance. Other perturbations that can cause postural hypotension include autonomic failure, as in dysautonomia, diabetes mellitus, and vasovagal syncope; increased venous compliance, as in hemodialysis; and reduced blood volume, as with space flight and prolonged bed rest. Several -adrenoceptor agonists are used to increase venous return in orthostatic intolerance; however, there is insufficient data to show that these drugs are more efficacious than placebo. Clearly, more basic science and clinical studies are needed to increase our knowledge and understanding of the venous system.     

Effects of head-up tilting on baroreceptor control in subjects with different tolerances to orthostatic stress

During orthostatic stress, an increase in peripheral vascular resistance normally results in arterial blood pressure being well maintained, despite a decrease in cardiac output. The present study was undertaken to determine whether the sensitivity of the carotid baroreceptor reflex was increased during orthostatic stress and whether failure to develop this increase was associated with poor orthostatic tolerance. Three groups of subjects were studied: asymptomatic controls; patients investigated for suspected posturally related syncope but who had normal responses to an orthostatic stress test (normal patients); and patients who were shown to have low orthostatic tolerance (early fainters). We determined responses of R-R interval and forearm vascular resistance (mean arterial pressure/brachial artery velocity by Doppler ultrasonography) to the loading and unloading of carotid baroreceptors by application of pressures of -30 and +30 mmHg to a chamber fitted over the neck. Responses were determined after 20 min of supine rest and after 10 min of head-up tilt at 60 degrees. Responses of cardiac interval were not significantly different between the three groups, and they were not altered by the postural change. Vascular responses also did not differ between the groups during supine rest. However, in healthy volunteers and in normal patients, responses to both neck suction and pressure were significantly enhanced during head-up tilt. In controls, responses to suction were increased by tilt from 0.04+/-0.1 to -1.01+/-0.2%.mmHg(-1) (means+/-S.E.M.; P<0.001) and those to neck pressure from -0.6+/-0.3 to -3.1+/-1.1%.mmHg(-1) (P<0.05). In the normal patients, the corresponding changes were: during suction, from -0.2+/-0.1 to -0.7+/-0.1%.mmHg(-1) (P<0.05); during pressure, from -0.7+/-0.1 to -1.5+/-0.3%.mmHg(-1) (P<0.05). In contrast, in patients with low orthostatic tolerance, posture had no effect on the reflex (neck suction, from -0.3+/-0.1 to -0.3+/-0.1%.mmHg(-1); neck pressure, from -1.0+/-0.3 to -0.9+/-0.2%.mmHg(-1)). We suggest that an increase in the sensitivity of the carotid baroreceptor/vascular resistance reflex may be important in the maintenance of blood pressure during orthostatic stress, and that failure of this to occur in patients with posturally related syncope may go some way towards explaining their poor orthostatic tolerance.     

The Usefulness of Head-Up Tilt Testing and Hemodynamic Investigations in the Workup of Syncope of Unknown Origin

To enhance the clinical evaluation of patients suffering from recurrent syncope of unknown origin, the integrity of mechanisms controlling blood pressure was examined in 151 patients utilizing a screening tilt test. Ninety-eight patients had an abnormal blood pressure and/or heart rate response to tilt testing, including provoked syncopal attacks in 63 patients. Whenever indicated, the screening tilt test was followed by blood volume and hemodynamic determinations, as well as autonomic nervous system testing to identify contributing pathophysiological abnormalities (hypovolemia, venous pooling, autonomic dysfunction). Detailed analysis of this battery of tests allowed us to conclude that: (1) The tilt test is commonly a provocative tool in the workup of patients with recurrent syncope due to vasovagal - vasodepressor reactions and other abnormalities of blood pressure regulation; (2) Its usefulness is augmented by associated hemodynamic and blood volume evaluations; (3) The identification of contributory pathophysiological mechanisms of blood pressure control facilitates specific therapeutic interventions.     

Interaction of cardiopulmonary and carotid baroreflex control of vascular resistance in humans.

Previous studies in experimental animals indicate an important inhibitory interaction between cardiopulmonary and arterial baroreflexes. In the dog, for example, cardiopulmonary vagal afferents modulate carotid baroreflex control of vascular resistance. On the other hand, previous studies in human subjects have not produced convincing evidence of a specific interaction between these baroreceptor reflexes. The purpose of this study was to determine whether unloading of cardiopulmonary baroreceptors in humans with nonhypotensive lower body negative pressure selectively augments the reflex vasoconstrictor responses to simulated carotid hypotension produced by neck pressure. In nine healthy subjects, we measured forearm vascular responses with plethysmography during lower body negative pressure alone (cardiopulmonary baroreflex), during neck pressure alone (carotid baroreflex), and during concomitant lower body negative pressure and neck pressure (baroreflex interaction). Lower body negative pressure produced a greater than twofold augmentation of the forearm vasoconstrictor response to neck pressure. This increase in resistance was significantly greater (P less than 0.05) than the algebraic sum of the increase in resistance from lower body negative pressure alone plus that from neck pressure alone. In contrast, lower body negative pressure did not potentiate the forearm vasoconstrictor responses either to intra-arterial norepinephrine or to the cold pressor test. Thus, the potentiation of the vasoconstrictor response to neck pressure by lower body negative pressure cannot be explained by augmented reactivity to the neurotransmitter or to a nonspecific augmentation of responses to all reflex vasoconstrictor stimuli. In conclusion, nonhypotensive lower body negative pressure selectively augments carotid baroreflex control of forearm vascular resistance. These experiments demonstrate a specific inhibitory cardiopulmonary-carotid baroreflex interaction in humans.     

Peripheral vascular responses during carotid baroreceptor stimulation in normotensive and hypertensive subjects

1. The carotid baroreceptors were stimulated for 2 min by neck suction at -30 and -60 mmHg in 19 normotensive subjects and 12 patients with moderate essential hypertension. 2. Blood pressure was measured with a mercury sphygmomanometer and heart rate was derived from beat-to-beat analysis of the electrocardiogram. Blood flow was measured simultaneously at calf and finger with venous occlusion plethysmography and the vascular resistance was calculated. 3. During neck suction at -30 and -60 mmHg there was a significant decrease in arterial blood pressure and heart rate. There was a transient vasodilatation of the calf blood vessels, while there was a sustained vasoconstriction of the finger blood vessels. These results were qualitatively similar in both groups; however, there were quantitative differences. 4. These experiments show that there is a selective autonomic control of the different peripheral vascular beds by the carotid baroreceptors in both normotension and mild essential hypertension.     

Reflex Inhibition of Renal Sympathetic Nerve Activity during Myocardial Ischemia Mediated by Left Ventricular Receptors with Vagal Afferents in Dogs

The major goal of this investigation was to determine if activation of cardiac receptors during coronary artery occlusion could inhibit efferent renal sympathetic nerve activity. In nine chloralose anesthetized dogs with only carotid (n = 3) or with sinoaortic (n = 6) baroreceptors operative, anterior descending coronary artery (LAD) occlusion resulted in a small decrease in mean arterial pressure (-9.8+/-5.1 mm Hg, NS) and in a significant (P < 0.05) increase in renal nerve activity (24.0+/-4.1%). In these dogs, circumflex coronary artery (Cx) occlusion resulted in greater hypotension (-18.4+/-4.0 mm Hg), and yet no change (1.1+/-9%) in renal nerve activity was noted. Changes in left atrial pressure during LAD and Cx occlusion were not different. In seven dogs with carotid sinus denervation, coronary occlusions resulted in decreases both in arterial pressure and in renal nerve activity which were consistently greater during Cx occlusion. The responses to coronary occlusion in six dogs after sinoaortic deafferentation were similar to those observed with only carotid sinuses denervated. In all experiments, vagotomy abolished the difference in the blood pressure responses and the decreases in renal sympathetic nerve activity during Cx occlusion. Vagotomy also abolished the decrease in nerve activity during LAD occlusion in dogs with carotid or sinoaortic denervation. These data show that Cx occlusion and, to a lesser degree, LAD occlusion resulted in reflex withdrawal of renal sympathetic nerve activity mediated by left ventricular receptors with vagal afferents. The reflex withdrawal of renal nerve activity during Cx occlusion occurred in spite of hypotension and the presence of functioning sinoaortic baroreceptors.     

Abnormal Vascular Responses to Exercise in Patients with Aortic Stenosis

We tested the hypothesis that the normal forearm vasoconstrictor response to leg exercise is inhibited or reversed in patients with aortic stenosis, possibly because of activation of left ventricular baroreceptors. Forearm vascular responses to supine leg exercise were measured in 10 patients with aortic stenosis and in 2 control groups of 6 patients with mitral stenosis and 5 patients without valvular heart disease.Forearm vasoconstriction occurred during exercise in the control groups. In contrast, forearm blood flow increased and forearm vascular resistance did not change in patients with aortic stenosis. In six patients with aortic stenosis and a history of exertional syncope, forearm vasodilatation occurred during the second minute of leg exercise. Inhibition or reversal of forearm vasoconstrictor responses in aortic stenosis was asscociated with significant increases in left ventricular pressure.In three patients with aortic stenosis and exertional syncope, forearm vasodilator responses to exercise changed to vasoconstrictor responses after aortic valve replacement.The results indicate that forearm vasoconstrictor responses to leg exercise are inhibited or reversed in patients with aortic stenosis, possibly because of activation of left ventricular baroreceptors. The observations suggest that reflex vasodilatation resulting from activation of left ventricular baroreceptors may contribute to exertional syncope in patients with aortic stenosis.     

维持性血液透析中患者低血压发生的原因分析及护理对策

目的分析维持性血液透析过程中患者低血压的发生原因,并提出相应的护理对策。方法回顾性调查和分析了本院自2009年12月-2010年1月90例(338例次)血液透析患者低血压发生的原因。结果低血压发生的主要原因为血容量不足、自主神经病变及器质性心脏疾病等。结论控制透析间期体重的增长,保证透析过程中有效循环血量的相对稳定及做好发生低血压时的紧急处理是保证血液透析顺利进行的关键。     

Neural Circulatory Control in Vasovagal Syncope

The orthostatic volume displacement associated with the upright position necessitates effective neural cardiovascular modulation. Neural control of cardiac chronograpy and inotropy, and vasomotor tone aims at maintaining venous return, thus opposing gravitational pooling of blood in the lower part of the body. The present concept of the vasovagal response or "common faint" implicates the development of inappropriate cardiac slowing due to sudden augmentation of efferent vagal activity, and arteriolar dilatation by sudden reduction or cessation of sympathetic activity. The venous pooling associated with lasting orthostatic stress results in development of central hypovolemia. At a certain point during the ongoing reflex adaptation to the hypovolemia in progress, a depressor reflex is set in train. The depressor reflex input along this second "peripheral" afferent pathway is postulated to originate from various sites in the cardiovascular system but remains uncertain. The common faint in humans is of both vaso- and vagal origin; the pure vagal response is less common than its vasodepressor variant. There is strong evidence for an early loss of vasomotor tone in the majority of fainting subjects. Blocking the vagus nerve or cardiac pacing is not of much help in preventing vasovagal syncope; though atropine or pacing may prevent bradycardia in vasovagal fainting, they have never been proven to prevent hypotension. Baroreflex modulation of autonomic outflow remains present during the presyncopal stages until it becomes offset by an opposing depressor reflex with relative bradycardia and relaxation of arterial resistance vessels. The nature of the vasodilatation associated with the vasovagal response has still not been settled.     

Haemodynamic consequences of experimental papillary necrosis in the rat

Experimental renal papillary necrosis induced by 2-bromoethylamine hydrobromide (BEA) results in hypertension in the rat. The haemodynamics of this increase in blood pressure were investigated with radiolabelled microspheres, thus enabling individual organ blood flows to be evaluated. Total peripheral resistance was raised in BEA-treated rats (3.6 +/- 0.3 mmHg ml-1 min X 100 g) compared with control rats (2.87 +/- SEM 0.2, P less than 0.05) whilst cardiac index remained similar (39.9 +/- 3.6 vs 39.2 +/- 3.1 ml min-1 100 g-1). Heart and brain from BEA rats demonstrated a significant rise in vascular resistance with a normal blood flow. In the kidneys vascular resistance increased still further and here there was a reduction in renal blood flow despite an increase in kidney size. These findings are compatible with a loss of renomedullary vasodepressor mechanisms acting directly or indirectly on the resistance vessels.     

ORAL DISOPYRAMIDE IN THE TREATMENT OF RECURRENT NEUROCARDIOGENIC SYNCOPE

In neurocardiogenic syncope the normal compensatory response on assuming an upright posture is interrupted after several minutes and replaced by a paradoxical withdrawal of sympathetic activity and increased parasympathetic activity. The resulting reduction in blood pressure is severe, sympathetic activity is inhibited, plasma norepinephrine levels do not increase and the heart rate decreases. The defect is a paradoxical interruption of sympathetic excitation associated with parasympathetic excitation, causing profound vasodilatation and bradycardia. Disopyramide has been shown not only to treat the bradycardia but also to control the hypotension.     

Investigation of various types of neurocardiogenic response to head-up tilting by extended hemodynamic and neurohumoral monitoring

BACKGROUND: The pathophysiology of neurocardiogenic syncope is heterogeneous. This study aim was to analyze whether extended monitoring during tilt-table testing provided additional information on the hemodynamic and vegetative state prior to neurocardiogenic syncope. METHODS: This retrospective analysis is based on data of head-up tilt-table testing of 40 unselected consecutive patients with a history of unexplained syncope. For optimized characterization of the type of syncope, monitoring included electrocardiogram (ECG), blood pressure measurements and cardiac output, peripheral vascular resistance and contractility index measurements by impedance cardiography, as well as epinephrine and norepinephrine plasma levels in supine position and every 5 min during tilting. RESULTS: Seven of 40 patients were unsuitable for analysis because of incomplete data sets. Tilt-table was positive in 26 patients, negative in 7. Groups did not differ in hemodynamic and catecholaminergic parameters at baseline. Responses to tilting were VASIS 1 (mix of cardioinhibitory and vasodepressor) in 5 patients, VASIS 2B (cardioinhibitory with asystole >3 sec) in 3, VASIS 3 (vasodepressor) in 16, orthostatic dysregulation in 2. In VASIS 1, the catecholamine measurement 4 min before syncope showed a proportionally larger increase of the epinephrine level than of norepinephrine. This disproportion was not observed in VASIS 2B and 3. In VASIS 2B, strong vasoconstriction and negative inotropy were evident in the presyncopal period. In VASIS 3, vascular resistance decreased continuously before syncope, while contractility index increased inadequately. Presyncopal epinephrine surge or norepinephrine loss was not observed in this group, suspecting other vasodilating factors. CONCLUSIONS: Extended monitoring by impedance cardiography and plasma catecholamine measurements during tilt-table testing gave further insight into different hemodynamic and neurohumoral presyncopal patterns among the various types of neurocardiogenic syncope and may thereby help to develop individualized therapeutic concepts.