Exercise hyperemia and vasoconstrictor responses in humans with cystic fibrosis.

ATP released from circulating erythrocytes is a potential signal regulating muscle blood flow during exercise (exercise hyperemia), and intravascular ATP appears to blunt sympathetic vasoconstriction during exercise. Erythrocytes from patients with cystic fibrosis (CF) do not release ATP. The goal of the present study was to determine whether increases in forearm blood flow during exercise are blunted in CF patients and whether CF patients exhibit greater vasoconstrictor responsiveness during exercise. Nine control subjects and 10 CF patients who were free of other disease complications (approximately 96% O2 saturation) performed incremental rhythmic forearm exercise at 5, 10, and 15% of maximum handgrip strength for 21 min (7 min at each workload). We used a cold pressor test to evoke sympathetic vasoconstriction under resting conditions and at each exercise workload. As a control, subjects performed a second exercise bout without the cold pressor test. Continuous brachial artery blood velocity was monitored beat-to-beat, and vessel diameter was assessed by Doppler ultrasound. Artery diameter, as well as blood pressure, heart rate, and O2 saturation, was measured at steady-state exercise and at 1 min into the cold pressor stimulus. Blood pressure and heart rate responses to the forearm exercise and each cold pressor test were similar in both groups (P > 0.05). Contrary to our hypothesis, forearm blood flow (P = 0.91) and forearm vascular conductance (P = 0.82) were similar at rest and at each level of exercise between CF patients and controls. Additionally, there was no difference in the degree of sympathetic vasoconstriction between groups at rest and at each level of exercise (P = 0.22). Our results suggest that ATP released from the deformation of erythrocytes is not an obligatory signal for exercise hyperemia in human skeletal muscle.     

Abnormal Neurovascular Control during Sympathoexcitation in Obesity

Objective: We tested the hypothesis that muscle sympathetic nerve activity (MSNA) and forearm vascular resistance (FVR) would be augmented during mental stress or cold pressor test in healthy obese individuals compared with healthy lean individuals. Research Methods and Procedures: Twenty‐nine healthy obese women and 12 age‐matched healthy lean women were involved in the study. MSNA was directly measured from the peroneal nerve using microneurography. Forearm blood flow was measured by venous occlusion plethysmography. Blood pressure (BP) was monitored noninvasively by an automatic BP cuff, and heart rate (HR) was measured by electrocardiogram. Stroop color word test was performed for 4 minutes, and the cold pressor test was performed for 2 minutes. Results: Baseline MSNA and FVR were greater in the obese group than in the lean group. BP and HR were similar between groups. During mental stress, MSNA and FVR were greater in obese individuals than in lean individuals, although the magnitude of response was similar between groups. BP and HR similarly increased in obese and lean individuals. During the cold pressor test, MSNA, FVR, and BP were greater in obese individuals, but the magnitude of response was similar between groups. HR increased similarly during the cold pressor test in both obese and lean individuals. Discussion: Obesity increases MSNA and FVR during mental stress and the cold pressor test. This inappropriate neurovascular control can be expected to have an adverse effect on the risk factors for cardiovascular events and, hence, should be considered in the treatment of obese patients.     

Gender affects sympathetic neurovascular control during postural stress

Sympathetic outflow increases during head-up tilt (HUT) to stabilize blood pressure in the presence of decreases in venous return and stroke volume (SV). Otherwise, orthostatic hypotension would develop. Gender differences in orthostatic tolerance have been noted but the mechanisms are still uncertain. More recently, Waters et al. reported in a limited sample, greater susceptibility of women to demonstrate orthostatic intolerance following space flight. Therefore, it is important to understand gender differences in reflex blood pressure regulation. Recently, we reported smaller increments in muscle sympathetic nerve activity (MSNA) in healthy women during graded HUT and a non-baroreflex cold pressor test. The purpose of this report is to examine the hypothesis that gender differences in blood pressure control during HUT are related to important variations in MSNA discharge patterns.     

Does the pressor response to ischemic exercise improve blood flow to contracting muscles in humans?

The purpose of this study was to determine in humans 1) the gain for the reflex pressor response that occurs when perfusion pressure to rhythmically contracting muscles is reduced and 2) whether the pressor response improves blood flow to the contracting muscles. Six normal subjects performed light, moderate, and heavy rhythmic forearm contractions (30/min) with the forearm enclosed in a Plexiglas box. Pressure in the box was increased 10 mmHg each minute up to 50 mmHg to reduce transmural pressure in the arterial system of the forearm. Mean arterial pressure (MAP) was measured continuously. During light exercise no reflex increase in MAP occurred until box pressure was 50 mmHg. During moderate and heavy exercise MAP began to increase with only 10- to 20-mmHg increases in box pressure. The slope of this increase was 3.5-3.9 mmHg per 10 mmHg of box pressure (approximately 60% of that in dogs). In a further study on six subjects a deep vein draining the active forearm muscles was cannulated and deep venous O2 saturation measured to assess how a 50-mmHg increase in box pressure and subsequent reflex increase in MAP altered blood flow to the contracting muscles during heavy rhythmic exercise. The increase in box pressure reduced blood flow to contracting forearm muscles by 20-25% and was followed by a 19-mmHg increase in MAP that did not appear to improve perfusion of the active muscles. This finding was unexpected, because studies in dogs suggest that the pressor response to rhythmic exercise with restricted muscle blood flow can improve perfusion of the active muscles.(ABSTRACT TRUNCATED AT 250 WORDS)     

Mechanisms of Responses of Systemic Circulation: Role of the Endothelial Factor of Vascular Tone Control

Experimental data on the effect of NO synthase inhibition on hemodynamic changes (blood pressure, cardiac output, and peripheral resistance) induced by an increased (polyglucin infusion) or decreased (orthostasis) cardiac output are presented. Under conditions of NO synthase inhibition, the pressor effects of polyglucin and orthostatic hypotension increased by 70 and 72%, respectively. The response of peripheral resistance had a similar trend. Significance of NO secretion by vascular endothelium for the development of systemic hemodynamic responses is proposed.     

Phenotypical evidence for a gender difference in cardiac norepinephrine transporter function

Norepinephrine transporter (NET) function has a central role in the regulation of synaptic norepinephrine concentrations. Clinical observations in orthostatic intolerance patients suggest a gender difference in NET function. We compared the cardiovascular response to selective NET inhibition with reboxetine between 12 healthy men and 12 age-matched women. Finger blood pressure, brachial blood pressure, and heart rate were measured. The subjects underwent cardiovascular autonomic reflex testing and a graded head-up tilt test. In a separate study, we applied incremental concentrations of tyramine and isoproterenol through subcutaneous microdialysis catheters in eight men and in eight women. NET inhibition elicited a threefold greater increase in supine blood pressure in men than women (P < 0.05). The pressor response was driven by an increased cardiac output. The orthostatic heart rate increase during NET inhibition was greater in men than women (56 +/- 5 beats/min in men, 42 +/- 4 beats/min in women, P < 0.001). In contrast, NET inhibition resulted in a similar suppression in the cold pressor and handgrip response, low-frequency blood pressure oscillations, and venous norepinephrine in the supine position. Men and women were similarly sensitive to the lipolytic effect of isoproterenol and tyramine. We conclude that NET inhibition results in more pronounced changes in cardiac regulation in men than women. Our observations suggest that the NET contribution to cardiac norepinephrine turnover may be decreased in women. The gender difference in NET function may not be expressed in tissues that are less NET dependent than the heart.     

Cardiovascular resistance to orthostatic load in athletes after aerobic exercise

Cardiovascular resistance to orthostatic load in the athletes in the 2-h recovery period after a prolonged aerobic exercise was studied. The response of the central (stroke volume and cardiac output) and peripheral blood volumes in the lower and upper extremities and abdominal and cervical regions in response to the tilt test before and during 2 h after exercise (30 min; heart rate, 156 ± 8 beats/min) was determined by the impedance method. It is found that (1) in the initial state before exercise, the blood flow distribution in favor of the cervical region in response to the tilt test was more efficient in the athletes, despite the decreased cardiac output, which was due to a large decrease in the blood flow in the lower extremities and an increased blood flow in the cervical region; (2) after exercise, the symptoms of potential orthostatic intolerance develop, such as postural hypotension, tachycardia, and reduced peripheral pulse blood volume, which were expressed in the standing position, and a reduced effectiveness of the blood flow distribution to the cervical region in the tilt test; and (3) the ability to effectively distribute the blood flow in favor of the cervical region in the athletes after exercise remained elevated, which was due to a large decrease in the blood flow in the abdominal region and in the lower extremities at the end of the recovery period.     

Camphor-Crataegus berry extract combination dose-dependently reduces tilt induced fall in blood pressure in orthostatic hypotension.

In order to test the efficacy of a combination of natural D-camphor and an extract of fresh crataegus berries (Korodin Herz-Kreislauf-Tropfen) on orthostatic hypotension, two similar, controlled, randomized studies were carried out in a balanced crossover design in 24 patients each with orthostatic dysregulation. The camphor-crataegus berry combination (CCC) was orally administered as a single regimen in 3 different dosages of 5 drops, 20 drops and 80 drops; a placebo with 20 drops of a 60% alcoholic solution served as control. Orthostatic hypotension was assessed with the tilt table test before and after medication. Source data of both studies were pooled and meta-analytically evaluated for all 48 patients. CCC drops decreased the orthostatic fall in blood pressure versus placebo, as almost uniformly established at all times by mean arterial pressure and diastolic blood pressure. Mean arterial pressure demonstrated the very fast onset of action by a clearly dose-dependent statistically significant effect even after 1-minute orthostasis. Increase of mean arterial pressure as compared to the orthostasis test before medication was on average 4.5 mmHg. CCC affected diastolic blood pressure after 1 minute of orthostasis in all dosages as compared to placebo. A statistically significant effect of the highest dose of 80 drops on diastolic blood pressure could be demonstrated after 1-, 3-, and 5-minute orthostasis. The hemodynamic findings of a stabilizing effect on arterial pressure in orthostasis corroborate the long-term medical experience with CCC and justify the indication orthostatic hypotension.     

Effects of prostaglandins E2, I2 and F2α, arachidonic acid and indomethacin on pressor responses to norepinephrine in conscious rats

The effects of prostaglandins E₂ (PGE₂), I₂ (PGI₂) and F₂α (PGF₂α), arachidonic acid and indomethacin on pressor responses to norepinephrine were examined in conscious rats. Intravenously infused PGE₂ (0.3, 1.25 μg/kg/min), PGI₂ (50, 100 ng/kg/min), PGF₂α (1.8, 5.4 μg/kg/min) and arachidonic acid (0.7, 1.4 mg/kg/min) did not change the basal blood pressure. Both PGE₂ and PGI₂ significantly attenuated pressor responses to norepinephrine, whereas PGF₂α significantly potentiated them. Arachidonic acid, a precursor of the prostaglandins (PGs), significantly attenuated pressor responses to norepinephrine. Since the attenuating effect of arachidonic acid was completely abolished by the pretreatment with indomethacin (5 mg/kg), arachidonic acid is thought to exert an effect through its conversion to PGs. On the contrary, intravenously injected indomethacin (0.2–5.0 mg/kg) facilitated pressor responses to norepinephrine in a dose-related manner without any direct effect on the basal blood pressure. These results suggest that endogenous PGs may participate in the regulation of blood pressure by modulating pressor responses to norepinephrine in conscious rats.     

Cardiovascular effects of the essential oil of Croton zehntneri leaves and its main constituents, anethole and estragole, in normotensive conscious rats

Cardiovascular effects of the essential oil of Croton zehntneri (EOCZ) were investigated in conscious rats. In these preparations, intravenous (i.v.) injections of EOCZ (1-20 mg kg(-1)) and its main constituents anethole and estragole (both at 1-10 mg kg(-1)) elicited brief and dose-dependent hypotension and bradycardia (phase I) that were followed by a significant pressor effect associated with a delayed bradycardia (phase II). The initial hypotension and bradycardia (phase I) of EOCZ were unchanged by atenolol (1.5 mg kg(-1), i.v.) or L-NAME (20 mg kg(-1), i.v.) pretreatment, but were respectively reversed into pressor and tachycardic effects by methylatropine (1 mg kg(-1), i.v.) pretreatment. The subsequent pressor effect and the delayed bradycardia (phase II) remained unaffected by atenolol, but were abolished by L-NAME and methylatropine pretreatment, respectively. In rat endothelium-containing aorta preparations, the vasoconstrictor responses to phenylephrine were enhanced and reduced, respectively, by the lower (1-30 microg mL(-1)) and higher (300-1000 microg mL(-1)) concentrations of EOCZ. Only the enhancement of phenylephrine-induced contraction was abolished by either the incubation with L-NAME (50 microM) or in the absence of the endothelium. These data show, for the first time, that i.v. administration EOCZ induces an initial hypotension followed by a pressor response, two effects that appear mainly attributed to the actions of anethole and estragole. The EOCZ-induced hypotension (phase I) is mediated by a cholinergic mechanism and seems to result mainly from the concomitant bradycardia. The pressor response of EOCZ (phase II) seems to be caused by an indirect vasoconstrictive action of EOCZ most likely through inhibition of endothelial nitric oxide production.     

Pindolol acts as beta-adrenoceptor agonist in orthostatic hypotension: therapeutic implications.

Three bedridden patients with severe orthostatic hypotension due to chronic autonomic failure were treated with pindolol (15 mg/day), a beta-adrenoceptor antagonist with partial agonist activity. While taking this drug the patients were free of orthostatic symptoms: they could walk, and standing blood pressure was maintained above 90/50 mm Hg. Supine heart rate rose during treatment by 12-21 beats/minute, and stroke volume and cardiac output by 12-24 ml and 1.5-3.1 l/min respectively. Supine blood pressure rose by 21-68 mm Hg systolic and 14-49 mm Hg diastolic. Pindolol 15 mg/day was therapeutically effective in these three patients with severe orthostatic hypotension due to chronic autonomic failure. Further studies in a larger series of patients are needed to confirm this result.     

Venous smooth muscle tone and responsiveness in older adults.

Venous compliance is lower in older adults compared with younger adults. It is possible that alterations in venous smooth muscle tone and responsiveness may contribute to the age-related differences in venous compliance. To determine the effects of sympathetic activation [cold pressor test (cold pressor test); rhythmic ischemic handgrip (rhythmic ischemic handgrip)] and endothelium-independent decreases in smooth muscle tone [sublingual nitroglycerin (nitroglycerin)] on venous compliance in young and older adults, forearm and calf venous compliance was measured in 12 young (22 +/- 1 yr) and 12 old (65 +/- 1 yr) supine subjects using venous occlusion plethysmography. Venous compliance was assessed at baseline, during the cold pressor test and rhythmic ischemic handgrip tests, and after nitroglycerin administration. All pressure-volume relationships were modeled with a quadratic regression equation, and beta1 and beta2 were used as indexes of venous compliance. A repeated-measures ANOVA was used to determine the effect of the age and trial on venous compliance. Calf regression parameters beta1 (0.0639 +/- 0.0126 vs. 0.0503 +/- 0.0059, young vs. older; P < 0.05) and beta2 (-0.00054 +/- 0.00011 vs. -0.00041 +/- 0.00005, young vs. older; P < 0.05) were significantly less in older adults at baseline. Similarly, forearm regression parameters, beta1 and beta2 were lower in older adults at baseline. Venous compliance was not effected by the cold pressor test test, rhythmic ischemic handgrip, or sublingual nitroglycerin in either group. Data suggest that forearm and calf venous compliance is lower in older adults compared with young. However, this difference probably cannot be explained by alterations in smooth muscle tone or responsiveness.     

The combined effect of the cold pressor test and isometric exercise on heart rate and blood pressure

The purpose of this study was to determine if the cold pressor test during isometric knee extension [15% of maximal voluntary contraction (MVC)] could have an additive effect on cardiovascular responses. Systolic and diastolic blood pressures, heart rate and pressure rate product were measured in eight healthy male subjects. The subjects performed the cold pressor tests and isometric leg extensions singly and in combination. The increases of systolic and diastolic blood pressure during isometric exercise were of almost the same magnitude as those during the cold pressor test. The responses of arterial blood pressure, and heart rate to a combination of the cold pressor test and isometric knee extension were greater than for each test separately. It is suggested that this additional effect of cold immersion of one hand during isometric exercise may have been due to vasoconstriction effects in the contralateral unstressed limb. In summary, the circulatory effects of the local application of cold during static exercise at 15% MVC were additive.     

Responses to whole body and finger cooling before and after an Antarctic expedition

Eight subjects, who were indoor workers and not habitually exposed to cold, spent 53 days in Antarctica. They did mainly geological field work often requiring the use of bare hands. The effects of the expedition on responses to a whole body cold exposure test, a finger blood flow test and a cold pressor test were studied. After the expedition, during whole-body cooling the time for the onset of shivering was delayed by 36 min (P<0.001) and forearm and thigh temperatures were 1.5°C higher (P<0.05) at the end of exposure. During local cooling of the finger with 10°C perfusion, finger vascular resistance was 14.9 (SEM 6.6) mmHg · ml^–1 · min · 100 ml (P<0.05) lower and finger temperature 3.9 (SEM 0.8) °C higher (P< 0.01). However, the decrease in rectal temperature during wholebody cooling was unaltered and the response to a cold pressor test was unchanged. The data would indicate that partial acclimatization to cold had been developed. Changes in forearm temperature were correlated with the duration of cold exposure of the hands (P < 0.05) and finger vascular resistance and finger temperature were correlated with responses to cooling before the expedition (P<0.001 and P<0.01, respectively). Because the ambient temperature was not clearly lower in Antarctica in comparison to Finland, the reason for the changes developed seems to be the increased exposure to the outdoor climate in Antarctica.     

刺激清醒大鼠躯体神经对失血性低血压的升压效应

在清醒雄性大鼠中经静脉抽出血液总量的约50%,造成失血性低血压。对照组大鼠在失血后不予处理。刺激组大鼠在失血后半小时用低频电脉冲刺激坐骨神经30min。刺激组动物的平均动脉压在刺激肘和刺激停止后2小时内均显著高于对照组。在同时记录内脏神经放电的动物中还看到,刺激坐骨神经时交感神经活动显著加强。这可能和血压、心率的恢复有关。在失血动物中刺激坐骨神经引起的升压效应不能被静脉内注射纳洛酮(8mg/kg)翻转;预先注射纳洛酮也不能阻断这种升压效应。在用水合氯醛麻醉的大鼠中,失血后刺激坐骨神经仍能引起升压反应。但如在刺激坐骨神经前静脉注射东莨菪碱(8—20mg/kg),则在多数动物中上述升压反应的幅度显著减小,甚至消失。实验结果表明,在失血性低血压的大鼠中,刺激坐骨神经可促进机体代偿反应,进一步加强交感神经活动,有利于血压的恢复。这一效应可能需要胆硷能递质参与,而内啡肽系统似乎不起重要作用。     

Leukotriene D4-induced hypotension is reversed by thyrotropin-releasing hormone

Injection of leukotriene D₄ (LTD₄, 20 μg/kg, i.a.) to conscious spontaneous hypertensive (SHR) rats produces a short-lasting pressor and tachycardic response followed by prolonged hypotension and bradycardia. Plasma norepinephrine and epinephrine were elevated at the peak pressor/tachycardic phase as well as at the hypotensive phase. Injection of thyrotropin-releasing hormone (TRH, 2 or 5 mg/kg) at the peak of the LTD₄-induced hypotension resulted in prompt reversal of the hypotension and bradycardia in a dose-related manner. Naloxone (5 mg/kg) had no effect on blood pressure and heart rate LTD₄- treated SHR rats. Pretreatment with TRH (5 mg/kg) did not prevent the depressor effect of LTD₄, but attenuated the bradycardic effect of this leukotriene. In addition, TRH had no effect on LTD₄-induced hypotension in the pithed SHR rat. These results suggest that TRH might exert beneficial effects in hypotensive states mediated by leukotrienes or other mediators of anaphylactic reactions.     

Effect of prenalterol on orthostatic hypotension in the Shy-Drager syndrome.

Treatment of idiopathic orthostatic hypotension is often unsatisfactory. A patient with the Shy-Drager syndrome, in which the most important symptom is orthostatic hypotension, was treated with prenalterol, initially 30 mg six times daily. The dosage was reduced to 30 mg four times daily because of the development of complex ventricular premature beats. Orthostatic symptoms were reduced and standing blood pressure increased. Fludrocortisone 0.5 mg a day was added to treatment with further improvement. This clinical effect was maintained throughout 12 months of follow up, during which the treatment was continued unchanged. Prenalterol was effective in reducing orthostatic symptoms in this patient. Further studies in patients with a similar haemodynamic pattern are indicated.     

Differences in action of topical and systemic cysteamine on gastric blood flow,gastric acid secretion and gastric ulceration in the rat

The effect of cysteamine on gastric blood flow and on the indomethacin-induced gastric mucosal damage was studied. In anesthetized rats, cysteamine (280 mg/kg) given subcutaneously (sc) decreased gastric blood flow measured by the laser Doppler flowmetry technique. In contrast, cysteamine (1–60 mg/ml) applied topically to the serosal surface of the stomach evoked a concentration-dependent and long-lasting increase in gastric blood flow. At 60 mg/ml, cysteamine increased blood flow by 166.8 ± 26.1% of predrug control value. Pretreatment with indomethacin (20 mg/kg, sc), intravenous (iv) atropine (1 mg/kg), propranolol (1 mg/kg, iv), combined H₁ and H₂-blockade or bilateral cervical vagotomy alone or combined with iv guanethidine (8 mg/kg), or pretreatment with the capsaicin analogue resiniferatoxin did not reduce the vasodilator response to cysteamine. The vasodilator response to topical capsaicin, was not reduced after sc cysteamine (280 mg/kg) pretreatment. In conscious pylorus-ligated rats, sc cysteamine (100 or 280 mg/kg) given simultaneously with indomethacin inhibited gastric acid output but had variable effects on the indomethacin-induced gastric mucosal damage. Cysteamine (100 or 280 mg/kg) administered sc 4 h prior to indomethacin enhanced gastric injury by sc indomethacin, but did not prevent the gastroprotective action of capsaicin. In contrast, orally administered cysteamine (60 mg/ml) reduced gastric injury induced by sc indomethacin plus intragastric HCl. These data provide the first evidence for the effect of cysteamine on gastric microcirculation in the rat and suggest a direct vasodilator effect for topical cysteamine. The microvascular effects of cysteamine are largely responsible for the different effects of this agent on experimental gastric injury.     

Effects of cyclo- and lipoxygenase inhibitors on hypoxic vasoconstriction in isolated ferret lungs

To evaluate the role of leukotrienes in hypoxic pulmonary vasoconstriction, we measured steady-state pressor responses to graded hypoxia in isolated ferret lungs perfused with autologous blood containing 0.001, 0.03, 1, or 3 mM nordihydroguaiaretic acid (NDGA), 1 mM BW 755C, or 0.02-0.05 mM indomethacin. Untreated lungs served as controls. Perfusate concentrations of thromboxane B2 and 6-ketoprostaglandin F1 alpha, measured by radioimmunoassay, were markedly reduced in all treated lungs, indicating inhibition of cyclooxygenase. The maximum pressor response to hypoxia measured at a blood flow of 50 ml.min-1. kg-1 averaged 26.6 +/- 2.4 Torr in untreated lungs and was not affected by BW 755C or 0.001-0.03 mM NDGA. Because BW 755C and NDGA inhibited cyclooxygenase at concentrations that did not affect hypoxic vasoconstriction and because both agents are thought to inhibit lipoxygenase with a potency greater than or equal to that with which they inhibit cyclooxygenase, these results do not support the possibility that hypoxic pulmonary vasoconstriction was mediated by leukotrienes. At concentrations of 1 and 3 mM, NDGA inhibited the maximum hypoxic pressor response by 57 and 95%, respectively. The mechanism of this attenuation is unknown; however, it was apparently not due to cyclooxygenase inhibition, since indomethacin enhanced the maximum hypoxic pressor response by 45%. Nor was it due to blockade of calcium entry or interference with the contractile process in pulmonary vascular smooth muscle, since 1 mM NDGA did not inhibit vasoconstrictor responses to KCl or prostaglandin F2 alpha.     

Pressor effect of electroacupuncture on hemorrhagic hypotension

Neiguan (PC-6) is a traditional acupoint in each forearm and overlies the trunk of the median nerve. Previous studies show that electroacupuncture (EA) at the Neiguan acupoint could improve not only myocardial ischemic dysfunction by inducing a depressor response but also recover hemorrhagic hypotension by inducing a pressor response. However, their physiological mechanisms are not yet elucidated. We investigated the pressor effect of Neiguan EA and its mechanism by focusing on left ventricular (LV) performance in a canine hemorrhagic hypotension model. We hemorrhaged 36 anesthetized and thoracotomized mongrel dogs and decreased LV end-systolic pressure (ESP) to approximately 70 mmHg (35% decrease). We obtained LV pressure-volume (P-V) data with a micromanometer catheter and a conductance catheter. One-hour Neiguan EA significantly recovered the decreased ESP, end-diastolic volume, and stroke volume by 32 +/- 13%, 27 +/- 13%, and 39 +/- 17%, respectively (P < 0.05), without changing heart rate and the slope of the end-systolic P-V relation. Neiguan EA inhibited a hemorrhage-induced increase in plasma catecholamines. However, vecuronium (neuromuscular blocking agent) administration abolished the antihypotension effect of Neiguan EA. Furthermore, Neiguan EA was much more effective than a nonacupoint thigh EA. We conclude that Neiguan EA achieved the antihypotension effect by improving LV filling of the hemorrhage-depressed LV performance despite the inhibition of the hemorrhage-increased plasma catecholamines. This pressor effect seemed to accompany an increased venous return by Neiguan EA-increased vasomotor tone and muscle pump. This study demonstrated a scientific basis for the therapeutic efficacy of acupuncture in the treatment of hemorrhagic hypotension and shock.