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At least 55 records · Page 3

Human cutaneous vascular responses to whole-body tilting, Gz centrifugation, and LBNP

We hypothesized that gravitational stimuli elicit cardiovascular responses in the following order with gravitational stress equalized at the level of the feet, from lowest to highest response: short-(SAC) and long-arm centrifugation (LAC), tilt, and lower body negative pressure (LBNP). Up to 15 healthy subjects underwent graded application of the four stimuli. Laser-Doppler flowmetry measured regional skin blood flow. At 0.6 G(z) (60 mmHg LBNP), tilt and LBNP similarly reduced leg skin blood flow to approximately 36% of supine baseline levels. Flow increased back toward baseline levels at 80-100 mmHg LBNP yet remained stable during 0.8-1.0 G(z) tilt. Centrifugation usually produced less leg vasoconstriction than tilt or LBNP. Surprisingly, SAC and LAC did not differ significantly. Thigh responses were less definitive than leg responses. No gravitational vasoconstriction occurred in the neck. All conditions except SAC increased heart rate, according to our hypothesized order. LBNP may be a more effective and practical means of simulating cardiovascular effects of gravity than centrifugation.

Motor Activity/physiology↗

Consequences of cardiovascular adaptation to spaceflight: implications for the use of pharmacological countermeasures

There is little evidence obtained from space flight to support the notion that occurrence of cardiac dysrhythmias, impaired cardiac and vascular function, and manifestation of asymptomatic cardiovascular disease represent serious risks during space flight. Therefore, the development of orthostatic hypotension and instability immediately after return from spaceflight probably reflect the most significant operational risks associated with the cardiovascular system of astronauts. Significant reductions in stroke volume and lower reserve for increasing peripheral vascular resistance contribute to ineffective maintenance of systemic arterial blood pressure during standing after spaceflight despite compensatory elevations in heart rate. The primary mechanism underlying reduced stroke volume appears to be a reduction in preload associated with less circulating blood volume while inadequate peripheral vasoconstriction may be caused partly by hyporeactivity of receptors that control arterial smooth muscle function. A focus for development of future countermeasures for hemodynamic responses to central hypovolemia includes the potential application of pharmacological agents that specifically target and restore blood volume (e.g., fludrocortisone, electrolyte-containing beverages) and reserve for vasoconstriction (e.g., midodrine, vasopressin). Based on systematic evaluations, acute physical exercise designed to elicit maximal effort or inspiratory resistance have shown promise as successful countermeasures that provide protection against development of orthostatic hypotension and intolerance without potential risks and side effects associated with specific pharmacological interventions.

Non-NASA Center↗

Baroreflex-mediated heart rate and vascular resistance responses 24 h after maximal exercise

INTRODUCTION: Plasma volume, heart rate (HR) variability, and stimulus-response relationships for baroreflex control of forearm vascular resistance (FVR) and HR were studied in eight healthy men after and without performing a bout of maximal exercise to test the hypotheses that acute expansion of plasma volume is associated with 1) reduction in baroreflex-mediated HR response, and 2) altered operational range for central venous pressure (CVP). METHODS: The relationship between stimulus (DeltaCVP) and vasoconstrictive reflex response (DeltaFVR) during unloading of cardiopulmonary baroreceptors was assessed with lower-body negative pressure (LBNP, 0, -5, -10, -15, -20 mm Hg). The relationship between stimulus (Deltamean arterial pressure (MAP)) and cardiac reflex response (DeltaHR) during loading of arterial baroreceptors was assessed with steady-state infusion of phenylephrine (PE) designed to increase MAP by 15 mm Hg alone and during application of LBNP (PE+LBNP) and neck pressure (PE+LBNP+NP). Measurements of vascular volume and autonomic baroreflex responses were conducted on two different test days, each separated by at least 1 wk. On one day, baroreflex response was tested 24 h after graded cycle exercise to volitional exhaustion. On another day, measurement of baroreflex response was repeated with no exercise (control). The order of exercise and control treatments was counterbalanced. RESULTS: Baseline CVP was elevated (P = 0.04) from a control value of 10.5 +/- 0.4 to 12.3 +/- 0.4 mm Hg 24 h after exercise. Average DeltaFVR/DeltaCVP during LBNP was not different (P = 0.942) between the exercise (-1.35 +/- 0.32 pru x mm Hg-1) and control (-1.32 +/- 0.36 pru x mm Hg-1) conditions. However, maximal exercise caused a shift along the reflex response relationship to a higher CVP and lower FVR. HR baroreflex response (DeltaHR/DeltaMAP) to PE+LBNP+NP was lower (P = 0.015) after maximal exercise (-0.43 +/- 0.15 beats x min-1 x mm Hg-1) compared with the control condition (-0.83 +/- 0.14 beats x min-1 x mm Hg-1). CONCLUSION: Expansion of vascular volume after acute exercise is associated with altered operational range for CVP and reduced HR response to arterial baroreceptor stimulation.

Non-NASA Center↗

Mechanisms of blood pressure regulation that differ in men repeatedly exposed to high-G acceleration

The purpose of this study was to test the hypothesis that repeated exposure to high acceleration (G) would be associated with enhanced functions of specific mechanisms of blood pressure regulation. We measured heart rate (HR), stroke volume (SV), cardiac output (), mean arterial blood pressure, central venous pressure, forearm and leg vascular resistance, catecholamines, and changes in leg volume (%DeltaLV) during various protocols of lower body negative pressure (LBNP), carotid stimulation, and infusions of adrenoreceptor agonists in 10 males after three training sessions on different days over a period of 5-7 days using a human centrifuge (G trained). These responses were compared with the same measurements in 10 males who were matched for height, weight, and fitness but did not undergo G training (controls). Compared with the control group, G-trained subjects demonstrated greater R-R interval response to equal carotid baroreceptor stimulation (7.3 +/- 1.2 vs. 3.9 +/- 0.4 ms/mmHg, P = 0.02), less vasoconstriction to equal low-pressure baroreceptor stimulation (-1.4 +/- 0.2 vs. -2.6 +/- 0.3 U/mmHg, P = 0.01), and higher HR (-1.2 +/- 0.2 vs. -0.5 +/- 0.1 beats. min(-1). mmHg(-1), P = 0.01) and alpha-adrenoreceptor response (32.8 +/- 3.4 vs. 19.5 +/- 4.7 U/mmHg, P = 0.04) to equal dose of phenylephrine. During graded LBNP, G-trained subjects had less decline in and SV, %DeltaLV, and elevation in thoracic impedance. G-trained subjects also had greater total blood (6,497 +/- 496 vs. 5,438 +/- 228 ml, P = 0.07) and erythrocyte (3,110 +/- 364 vs. 2,310 +/- 96 ml, P = 0.06) volumes. These results support the hypothesis that exposure to repeated high G is associated with increased capacities of mechanisms that underlie blood pressure regulation.

Non-NASA Center↗

Steady-state temperature distribution in living tissue modeled as cylindrical shells.

Closed form, analytical solutions to the problem of steady-state heat transfer in living tissue modeled as cylindrical shells are presented and discussed. These solutions are particularly useful for the study of temperature distributions in the extremities. Metabolic heat generation, conduction, and heat transported by the blood perfusing the tissue are considered in the model. The results demonstrate the important role that the blood stream plays in the transfer of heat inside living tissue. Solutions are also presented for the limiting cases of diminishing blood flow that would occur during vasoconstriction or occlusion of blood by external means.

Shitzer, A.↗

Effects of noise upon human information processing

Studies of noise effects upon human information processing are described which investigated whether or not effects of noise upon performance are dependent upon specific characteristics of noise stimulation and their interaction with task conditions. The difficulty of predicting noise effects was emphasized. Arousal theory was considered to have explanatory value in interpreting the findings of all the studies. Performance under noise was found to involve a psychophysiological cost, measured by vasoconstriction response, with the degree of response cost being related to scores on a noise annoyance sensitivity scale. Noise sensitive subjects showed a greater autonomic response under noise stimulation.

Cohen, H. H.↗

Reflex limb dilatation following norepinephrine and angiotensin II in conscious dogs

The extent to which norepinephrine (NE) and angiotensin II (AN) constrict the mesenteric, renal, and iliac beds in conscious dogs is evaluated with a view to elicit opposing reflex actions tempering the vasoconstriction in the limb of the animals tested. The afferent and efferent mechanisms mediating this reflex are analyzed. It is shown that intravenous NE and AN cause striking reflex iliac dilatation in the limb of the conscious dog. The afferent arc of this reflex involves both arterial baroreceptor and vagal path-ways, whereas the efferent mechanism involves an interaction of alpha-adrenergic and histaminergic receptors.

Vatner, S. F.↗

Mechanisms of radio-protection by catecholamines in the hamster /Mesocricetus auratus/

Experiments were conducted on normal and splenectomized male and female hamsters between 2 and 3 months old subjected to a whole-body exposure of 1000 or 2000 rads in a Co-60 source with a view toward evaluating their radio-protection by norepinephrine, isoproterenol, and phenylephrine. Vasoconstriction hypoxia mechanism of radio-protection is examined along with the hypothesis that isoproterenol protects by hypercalcemia-induced cell proliferation. Radiation experiment results are found to be consistent with the hypothesis that stimulation of alpha receptors results in radio-protection through a tissue hypoxia mechanism. Beta agonists seem to protect by a hypotensive-hypoxia mechanism. The catecholamines protect against the hematopoietic syndrome, but show no evidence of protection against the gastrointestinal syndrome.

Prewitt, R. L.↗

Gravitational haemodynamics and oedema prevention in the giraffe

The question of how giraffes avoid pooling of blood and tissue fluid (edema) in dependent tissues of their extremities is addressed. As monitored by radiotelemetry, the blood and tissue fluid pressures that govern transcapillary exchange vary greatly with exercise. These pressures, combined with a tight skin layer, move fluid upward against gravity. The skin thus functions like a natural antigravity suit. Other mechanisms that prevent edema include precapillary vasoconstriction and low permeability of capillaries to plasma proteins.

Hargens, Alan R.↗

Leg vascular responsiveness during acute orthostasis following simulated weightlessness

The effect of weightlessness on vascular response to orthostatic stress was investigated in human subjects by measuring changes in the arterial pulse volume (APV) of the legs during exposure to lower body negative pressure (LBNP) applied before and after 10 days of continuous 6-deg head-down bed rest. Heart rate, mean arterial blood pressure (MAP), and impedance rheographic indices of APV were measured during rest and at 1 min of -30 mm Hg LBNP. Bed rest was found not to alter the responses of MAP to LBNP. Resting APV was decreased after bed rest; however, APV was reduced upon transfer from rest to 1-min LBPN by the same relative magnitude before and after bedrest. It is concluded that peripheral arterial vasoconstriction, as indicated by reduction in APV during LBNP, is not affected by bedrest. The results suggest that there was no apparent alteration in responsiveness of the leg vasculature following simulated weightlessness, and that the control mechanisms of peripheral resistance do not contribute significantly to reduced orthostatic tolerance following spaceflight.

Blamick, Cynthia A.↗

Human circulatory responses to prolonged hyperbaric hyperoxia in Predictive Studies V

Selected results of cardiocirculatory measurements in healthy volunteers who breathed 100 percent O2 continuously at 3.0 ATA for up to 3.5 hr, at 2.5 ATA for up to 6.0 hr, at 2.0 ATA for up to 11.9 hr, and at 1.5 ATA for up to 19.0 hr are reported. The results indicate that resting hemodynamic responses to prolonged hyperbaric oxygen breathing in man usually consist of small deviations from normal sea-level responses. Rapid onset of bradycardia occurred at all four oxygen pressures investigated. This effect was accompanied by a rate-dependent reduction in cardiac output and a degree of systematic vasoconstriction which were small in magnitude and appeared to be functionally unimportant.

Pisarello, J. B.↗

Altered baseline blood volume and the norepinephrine response to stress in humans

A hypothesis is proposed that a primary physiological purpose of the neural and endocrine response to stressors is the preservation of the blood volume/blood pressure relationship. Changes in blood volume caused by an adaptation to the environmental challenge serve to modulate the neural and endocrine responsiveness to stress. Relationships between changes in vascular volume, vasoconstriction, and norepinephrine (NE) responses during acute and chronic exposure to various stressors are examined. It is noted that the hypothesis is based on numerous observations rather than definitive cause-effect experiments and further investigation is required to prove it.

Vernikos, J.↗

Drug effects on orthostatic intolerance induced by bedrest

Effective and practical preventive procedures for postflight orthostatic intolerance are highly desirable. The current practice of attempts to expand plasma volume by ingestion of salt and fluids before reentry has proven benefits. This study evaluated alternative options using fludrocortisone (F) to expand plasma volume (PV), dextroamphetamine (Dex) to enhance norepinephrine (NE) release, and atropine (A) to reduce the effects of vagal stimulation. Seven subjects with proven post-bedrest orthostatic intolerance returned for a 7-day 6-deg head-down bedrest study. F (0.2 mg) was given at 8:00 AM and 8:00 PM the day before and 8:00 AM the day the subjects got out of bed (2 hours before standing). PV was measured before and 1 hour after the last dose of F. Dex (5 mg) and A (0.8 mg) were then taken orally 1 hour before the stand test. F expanded PV by 16 percent and caused sodium retention. Four of the 7 subjects stood for 1 hour post-bedrest and heart rate, plasma NE and plasma renin responses to standing were greatly enhanced and sustained. Although there was a narrowing of pulse pressure, the ability to overcome orthostatic intolerance with these countermeasures was largely due to vasoconstriction and sustained high heart rate.

Vernikos, J.↗

Alterations in Skeletal Muscle Microcirculation of Head-Down Tilted Rats

In this study we assessed the function of microscopic blood vessels in skeletal muscle (cremaster muscle) for alterations which may contribute to the observed elevation of blood pressure associated with head-down tilted whole body suspension (HDT/WBS), a model of weightlessness. Arteriolar baseline diameters, vasoconstrictor responses to norepinephrine (NE) and vasodilation to nitroprusside (NP) were assessed in control rats, rats suspended for 7 or 14 day HDT/WBS rats, and rats allowed to recover for 1 day after 7 days HDT/WBS. Neither baseline diameters nor ability to dilate were influenced by HDT/WBS. Maximum vasoconstriction to norepinephrine was significantly greater in arterioles of hypertensive 14 day HDT/WBS rats. This first study of the intact microvasculature in skeletal muscle indicates that an elevated contractility of arterioles to norepinephrine in suspended rats, and suggests an elevated peripheral resistance in striated muscle may contribute to the increase in blood pressures among animals subjected to HDT/WBS.

Musacchia, X. J.↗

Diminished Baroreflex Control of Forearm Vascular Resistance Following Training

The stimulus-response characteristics of cardiopulmonary baroreflex control of forearm vascular resistance (FVR units in mm Hg x min x I00 ml/ml) were studied in 14 volunteers before and after 10 wk of endurance training. We assessed the relationship betaleen reflex stimulus (changes in central venous pressure, CVP) and response (FVR) during unloading of cardiopulmonary baroreceptors with lower body negative pressure (LBNP, 0 to - 2O mm Hg). Changes in CVP during LBNP were estimated from pressure changes in a large peripheral vein in the dependent arm of the subject in the right lateral decubitus position. Maximal oxygen uptake (VO(sub 2max)) and total blood volume increased with endurance training from 37.8 +/- 1.4 ml/min x kg and 63.6 +/- 2.1 ml/kg to 45.3 +/- 1.4 ml/ min x kg and 69.3 +/- 2.8 ml/kg respectively (P less than 0.05). Reflex forearm vasoconstriction occurred in response to a reduction in estimated CVP, and the absolute change in FVR per unit of CVP was reduced from -5.96 +/- 0.79 to -4.06 +/- 0.52 units x mm/ Hg (P less than 0.05) following exercise training but was unchanged from -6.10 to 0.57 to -6.22 +/- 0.94 units x mm/ Hg for the time control group (N = 7). Resting values for FVR were similar before and after exercise training; however, resting estimated CVP was elevated from 9.5 +/- 0.5 mm x Hg before training to 11.3 +/- 0.6 mm x Hg after training. The reduction in sensitivity of the cardiopulmonary baroreflex control of FVR was linearly related to the increase in blood volume (r = 0.65, P less than 0.05). suggesting that diminished cardiopulmonary baroreflex control of FVR in physically fit individuals is related, in part, to a training-induced blood volume expansion.

Mack, G. W.↗

Leg Vascular Responsiveness During Acute Orthostasis Following Simulated Weightlessness

Ten men (35-49 years old) underwent lower body negative pressure (LBNP) exposures before and offer 10 d of continuous 6 degrees head-down bedrest in order to predict the effect of weightlessness on the responsiveness of leg vasculature to an orthostatic stress. Heart rate (HR), mean arterial blood pressure (MAP), and Impedance rheographic indices of arterial pulse volume (APV) of the legs were measured during rest and at 1 min at -30 mm Hg LBNP. Bedrest-induced deconditioning was manifested by decreases (p less than 0.06) in plasma volume (17%), peak oxygen uptake (16%), and LBNP tolerance (17%). Resting HR was unchanged after bedrest, but HR was higher (p less than 0.05) at 1 min of -30 mm Hg LBNP after, compared with before bedrest. Responses of MAP to -30 mm Hg LBNP were not altered by bodrest. Resting APV was decreased (p less than 0.05) by simulated weightlessness. However, APV was reduced (p less than 0.05) from rest to 1 min -30 mm Hg LBNP by the same relative magnitude before and after bodrest (-21.4 +/- 3.4% and -20.5 +/- 2.7%, respectively). We conclude that peripheral arterial vasoconstriction, as indicated by reductions in APV during LBNP, was not affected by bedrest. These results suggest that there was no apparent alteration in responsiveness of the leg vasculature following simulated weightlessness. Therefore, it appears unlikely that control mechanisms of peripheral resistance contribute significantly to reduced orthostatic tolerance following space-flight.

Blamick, Cynthia A.↗

Corticosterone, but not Glucose, Treatment Enables Fasted Adrenalectomized Rats to Survive Moderate Hemorrhage

Fed adrenalectomized rats survive the stress of hemorrhage and hypovolemia, whereas fasted adrenalectomized rats become hypotensive and hypoglycemic after the first 90 min and die within 4 hours (h). We have studied the effects of glucose and corticosterone (B) infusions after hemorrhage as well as treatment with B at the time of adrenalectomy on the capacity of chronically prepared, conscious, fasted, adrenalectomized rats to survive hemorrhage. We have also measured the magnitudes of vasoactive hormone responses to hemorrhage. Maintenance of plasma glucose concentrations did not sustain life; however, treatment of rats at the time of adrenalectomy with B allowed 100 percent survival, and acute treatment of adrenalectomized rats at the time of hemorrhage allowed about 50 percent survival during the 5-h posthemorrhage observation period. Rats in the acute B infusion group that died exhibited significantly increased plasma B and significantly decreased plasma glucose concentrations by 2 h compared to the rats that lived. Plasma vasopressin, renin, and norepinephrine responses to hemorrhage were markedly augmented in the adrenalectomized rats not treated with B, and plasma vasopressin concentrations were significantly elevated at 1 and 2 h in all of the rats that subsequently died compared to values in those that lived. We conclude that: 1) death after hemorrhage in fasted adrenalectomized rats is not a result of lack of glucose; 2) chronic and, to an extent, acute treatment of fasted adrenalectomized rats with B enables survival; 3) fasted adrenalectomized rats exhibit strong evidence of hepatic insufficiency which is not apparent in either fed adrenalectomized rats or B-treated fasted adrenalectomized rats; 4) death after hemorrhage in fasted adrenalectomized rats may result from hepatic failure as a consequence of marked splanchnic vasoconstriction mediated bv the actions of extraordinarily high levels of vasoactive hormones after hemorrhage; and 5) B appears to act to decrease the magnitude of response of vasoactive hormones after hemorrhage in fasted adrenatectomized rats.

Darlington, Daniel N.↗