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At least 37 records · Page 2
All sourcesNASA NTRSDOE OSTI
NASA NTRS1999

Physiologic Pressure and Flow Changes During Parabolic Flight (Pilot Study)

The objective of this study was to obtain measurement of cutaneous tissue perfusion central and peripheral venous pressure, and esophageal and abdominal pressure in human test subjects during parabolic flight. Hemodynamic data recorded during SLS-I and SLS-2 missions have resulted in the paradoxical finding of increased cardiac stroke volume in the presence of a decreased central venous pressure (CVP) following entry in weightlessness. The investigators have proposed that in the absence of gravity, acceleration-induced peripheral vascular compression is relieved, increasing peripheral vascular capacity and flow while reducing central and peripheral venous pressure, This pilot study seeks to measure blood pressure and flow in human test subjects during parabolic flight for different postures.

Pantalos, George↗
NASA NTRS1995

Cardiovascular and Body Fluid Adjustments During Bed Rest and Space Flight

Although a few scientific bed rest (BR) studies were conducted soon after World War II, advent of the space program provided impetus for utilizing prolonged (days-months) BR, which employed the horizontal or 6 degree head-down tilt (HDT) body positions, to simulate responses of healthy people to microgravity. Shorter (hours) HDT protocols were used to study initial mechanisms of the acclimation-deconditioning (reduction of physical fitness) syndromes. Of the major physiological factors modified during BR, reduced force on bones, ligaments, and muscles, and greatly reduced hydrostatic pressure within the cardiovascular system, the latter: which involves shifts of blood from the lower extremities into the upper body, increase in central venous pressure, and diuresis, appears to be the initial stimulus for acclimation. Increase in central venous pressure occurs in subjects during weightless parabolic flight, but not in astronauts early during orbital flight. But significant reduction in total body water (hypohydration) and plasma volume (hypovolemia) occurs in subjects during both BR and microgravity. Response of interstitial fluid volume is not as clear, It has been reported to increase during BR, and it may have increased in Skylab II and IV astronauts. Reduction of total body water, and greater proportional reduction of extracellular volume, indicates increased cellular volume which may contribute to inflight cephalic edema. Cerebral pressure abates after a few days of HDT, but not during flight. accompanied by normal (eugravity) blood constituent concentrations suggesting some degree of acclimation had occurred. But during reentry, with moderately increased +Gz (head-to-foot) acceleration and gravitational force, the microgravity "euhydration" becomes functional progressive dehydration contributing to the general reentry syndrome (GRS) which, upon landing the Shuttle, can and often results in gastrointestinal distress, disorientation, vertigo, fatigue, and fainting. Various pre-reentry hyperhydration procedures have been utilized to counteract the GRS. Thus, the somewhat decreased central venous pressure and lack of diuresis early in spaceflight suggests mechanisms other than the Gauer-Henry reflex are more important for maintaining fluid volume homeostasis in astronauts. Inflight hypohydration and hypovolemia are more important for maintaining fluid volume homeostasis in astronauts.

Greenleaf, John E.↗
NASA NTRS1974

Venous return curves obtained from graded series of valsalva maneuvers

The effects were studied of a graded series of valsalva-like maneuvers on the venous return, which was measured transcutaneously in the jugular vein of an anesthetized dog, with the animal serving as its own control. At each of five different levels of central venous pressure, the airway pressure which just stopped venous return during each series of maneuvers was determined. It was found that this end-point airway pressure is not a good estimator of the animal's resting central venous pressure prior to the simulated valsalva maneuver. It was further found that the measured change in right atrial pressure during a valsalva maneuver is less than the change in airway pressure during the same maneuver, instead of being equal, as had been expected. Relative venous return curves were constructed from the data obtained during the graded series of valsalva maneuvers.

Mastenbrook, S. M., Jr.↗
NASA NTRS1995

Cardiovascular Pressures with Venous Gas Embolism and Decompression

Venous gas embolism (VGE) is reported with decompression to a decreased ambient pressure. With severe decompression, or in cases where an intracardiac septal defect (patent foramen ovale) exists, the venous bubbles can become arterialized and cause neurological decompression illness. Incidence rates of patent foramen ovale in the general population range from 25-34% and yet aviators, astronauts, and deepsea divers who have decompression-induced venous bubbles do not demonstrate neurological symptoms at these high rates. This apparent disparity may be attributable to the normal pressure gradient across the atria of the heart that must be reversed for there to be flow potency. We evaluated the effects of: venous gas embolism (0.025, 0.05 and 0.15 ml/ kg min for 180 min.) hyperbaric decompression; and hypobaric decompression on the pressure gradient across the left and right atria in anesthetized dogs with intact atrial septa. Left ventricular end-diastolic pressure was used as a measure of left atrial pressure. In a total of 92 experimental evaluations in 22 dogs, there were no reported reversals in the mean pressure gradient across the atria; a total of 3 transient reversals occurred during the peak pressure gradient changes. The reasons that decompression-induced venous bubbles do not consistently cause serious symptoms of decompression illness may be that the amount of venous gas does not always cause sufficient pressure reversal across a patent foramen ovale to cause arterialization of the venous bubbles.

Butler, B. D.↗
NASA NTRS1986

Continuous blood densitometry - Fluid shifts after graded hemorrhage in animals

Rapid fluid shifts in four pigs and two dogs subjected to graded hemorrhage are investigated. Arterial blood density (BD), mean arterial pressure (MAP), central venous pressure (CVP), arterial plasma density (PD), hematocrit (Hct) and erythrocyte density were measured. The apparatus and mechancial oscillator technique for measuring density are described. Fluid shifts between red blood cells and blood plasma and alterations in the whole-body-to-large vessel Hct, F(cell) are studied using two models. The bases of the model calculations are discussed. A decrease in MAP, CVP, and BP is detected at the beginning of hemorrhaging; continued bleeding results in further BD decrease correlating with volume displacement. The data reveal that at 15 ml/kg blood loss the mean PD and BD dropped by 0.99 + or - 0.15 and 2.42 + or 0.26 g/liter, respectively, and the Hct dropped by 2.40 + or 0.47 units. The data reveal that inward-shifted fluid has a higher density than normal ultrafiltrate and/or there is a rise in the F(cell) ratio. It is noted that rapid fluid replacement ranged from 5.8 + or - 0.8 to 10.6 + or - 2.0 percent of the initial plasma volume.

Hinghofer-Szalkay, H.↗
NASA NTRS1997

Cardiovascular consequences of bed rest: effect on maximal oxygen uptake

Maximal oxygen uptake (VO2max) is reduced in healthy individuals confined to bed rest, suggesting it is independent of any disease state. The magnitude of reduction in VO2max is dependent on duration of bed rest and the initial level of aerobic fitness (VO2max), but it appears to be independent of age or gender. Bed rest induces an elevated maximal heart rate which, in turn, is associated with decreased cardiac vagal tone, increased sympathetic catecholamine secretion, and greater cardiac beta-receptor sensitivity. Despite the elevation in heart rate, VO2max is reduced primarily from decreased maximal stroke volume and cardiac output. An elevated ejection fraction during exercise following bed rest suggests that the lower stroke volume is not caused by ventricular dysfunction but is primarily the result of decreased venous return associated with lower circulating blood volume, reduced central venous pressure, and higher venous compliance in the lower extremities. VO2max, stroke volume, and cardiac output are further compromised by exercise in the upright posture. The contribution of hypovolemia to reduced cardiac output during exercise following bed rest is supported by the close relationship between the relative magnitude (% delta) and time course of change in blood volume and VO2max during bed rest, and also by the fact that retention of plasma volume is associated with maintenance of VO2max after bed rest. Arteriovenous oxygen difference during maximal exercise is not altered by bed rest, suggesting that peripheral mechanisms may not contribute significantly to the decreased VO2max. However reduction in baseline and maximal muscle blood flow, red blood cell volume, and capillarization in working muscles represent peripheral mechanisms that may contribute to limited oxygen delivery and, subsequently, lowered VO2max. Thus, alterations in cardiac and vascular functions induced by prolonged confinement to bed rest contribute to diminution of maximal oxygen uptake and reserve capacity to perform physical work.

Non-NASA Center↗
NASA NTRS1996

Cardiovascular adaptation to spaceflight

This article reviews recent flight and ground-based studies of cardiovascular adaptation to spaceflight. Prominent features of microgravity exposure include loss of gravitational pressures, relatively low venous pressures, headward fluid shifts, plasma volume loss, and postflight orthostatic intolerance and reduced exercise capacity. Many of these short-term responses to microgravity extend themselves during long-duration microgravity exposure and may be explained by altered pressures (blood and tissue) and fluid balance in local tissues nourished by the cardiovascular system. In this regard, it is particularly noteworthy that tissues of the lower body (e.g., foot) are well adapted to local hypertension on Earth, whereas tissues of the upper body (e.g., head) are not as well adapted to increase in local blood pressure. For these and other reasons, countermeasures for long-duration flight should include reestablishment of higher, Earth-like blood pressures in the lower body.

Review, Tutorial↗
NASA NTRS1994

Cardiovascular regulation in humans in response to oscillatory lower body negative pressure

The frequency response characteristics of human cardiovascular regulation during hypotensive stress have not been determined. We therefore exposed 10 male volunteers to seven frequencies (0.004-0.1 Hz) of oscillatory lower body negative pressure (OLBNP; 0-50 mmHg). Fourier spectra of arterial pressure (AP), central venous pressure (CVP), stroke volume (SV), cardiac output (CO), heart rate (HR), and total peripheral resistance (TPR) were determined and first harmonic mean, amplitude, and phase angles with respect to OLBNP are presented. AP was relatively well regulated as demonstrated by small oscillations in half amplitude (3.5 mmHg) that were independent of OLBNP frequency and similar to unstressed control spectra. Due to the biomechanics of the system, the magnitudes of oscillations in calf circumference (CC) and CVP decreased with increasing frequency; therefore, we normalized responses by these indexes of the fluid volume shifted. The ratios of oscillations in AP to oscillations in CC increased by an order of magnitude, whereas oscillations in CVP to oscillations in CC and oscillations in AP to oscillations in CVP both tripled between 0.004 and 0.1 Hz. Therefore, even though the amount of fluid shifted by OLBNP decreased with increasing frequency, the magnitude of both CVP and AP oscillations per volume of fluid shifted increased (peaking at 0.08 Hz). The phase relationships between variables, particularly the increasing lags in SV and TPR, but not CVP, indicated that efferent responses with lags of 5-6 s could account for the observed responses. We conclude that, at frequencies below 0.02 Hz, the neural system of humans functioned optimally in regulating AP; OLBNP-induced decreases in SV (by as much as 50%) were counteracted by appropriate oscillations in HR and TPR responses. As OLBNP frequency increased, SV, TPR, and HR oscillations increasingly lagged the input and became less optimally timed for AP regulation.

NASA Discipline Cardiopulmonary↗
NASA NTRS1993

Circulatory filling pressures during transient microgravity induced by parabolic flight

Theoretical concepts hold that blood in the gravity dependent portion of the body would relocate to more cephalad compartments under microgravity. The result is an increase in blood volume in the thoraic and cardiac chambers. However, experimental data has been somewhat contradictory and nonconclusive. Early studies of peripheral venous pressure and estimates of central venous pressure (CVP) from these data did not show an increase in CVP under microgravity. However, CVP recorded in human volunteers during a parabolic flight revealed an increase in CVP during the microgravity state. On the STS 40 shuttle mission, a payload specialist wore a fluid line that recorded CVP during the first few hours of orbital insertion. These data revealed decreased CVP. When this CVP catheter was tested during parabolic flight in four subjects, two had increased CVP recordings and two had decreased CVP measurements. In 1991, our laboratory performed parabolic flight studies in several chronic-instrumented baboons. It was again noted that centrally recorded right atrial pressure varied with exposure to microgravity, some animals having an increase, and others a decrease.

Latham, Ricky D.↗
NASA NTRS1990

Baroreflex Responses to Acute Changes in Blood Volume in Humans

To test the hypothesis that acute changes in plasma volume affect the stimulus-response relations of high- and low- pressure baroreflexes, eight men (27-44 yr old) underwent measurements for carotid-cardiac and cardiopulmonary baro-reflex responses under the following three volemic conditions: hypovolemic, normovolemic, and hypervolemic. The stimulus- response relation of the carotid-cardiac response curve was generated using a neck cuff device, which delivered pressure changes between +40 and -65 mmHg in continuous steps of 15 mmHg. The stimulus-response relationship, of the cardio-pulmonary baroreflex were studied by measurements of Forearm Vascular Resistance (FVR) and Peripheral Venous Pressure (PVP) during low levels of lower body negative pressure (O to -20 mmHg). The results indicate greater demand for vasoconstriction for equal reductions in venous pressure during progressive hypovolemia; this condition may compromise the capacity to provide adequate peripheral resistance during severe orthostatic stress. Fluid loading before reentry after spaceflight may act to restore vasoconstrictive capacity of the cardiopulmonary baroreflex but may not be an effective countermeasure against potential post- flight impairment of the carotid-cardiac baroreflex.

Thompson, Cynthia A.↗
NASA NTRS1986

Mechanism for negative water balance during weightlessness An hypothesis

The mechanism for the apparent decrease in body fluid volume in astronauts during spaceflight remains obscure. The widespread postulate that the hypohydration is the result of the Henry-Gauer reflex, a diuresis caused by inhibition of vasopressin secretion resulting from increased left and perhaps right atrial (central) venous pressure, has not been established with direct measurements on astronauts. An hypothesis is proposed to account for fluid-electrolyte shifts during weightlessness. A moderate but transient increase in central venous pressure occurs when orbit is entered that is insufficient to activate the Henry-Gauer reflex but sufficient to stimulate the release of atrial natriuretic peptides. Increased sodium excretion would facilitate some increased urinary water loss. The resulting relatively dilute plasma and interstitial fluids would cause fluid to shift into the cellular space, resulting in edema in the head and trunk and inhibition of thirst and drinking. Thus, the negative water balance in astronauts would be caused by a gradual natriuresis and diuresis coupled with reduced fluid intake.

Greenleaf, J. E.↗
NASA NTRS1979

Cardiovascular regulatory response to lower body negative pressure following blood volume loss

An attempt is made to explain the cardiovascular regulatory responses to lower body negative pressure (LBNP) stress, both in the absence of and following blood or plasma volume loss, the latter being factors regularly observed with short- or long-term recumbency or weightlessness and associated with resulting cardiovascular deconditioning. Analytical expressions are derived for the responses of mean venous pressure and blood volume pooled in the lower body due to LBNP. An analysis is presented for determining the HR change due to LBNP stress following blood volume loss. It is concluded that the reduced orthostatic tolerance following long-term space flight or recumbency can be mainly attributed to blood volume loss, and that the associated cardiovascular responses characterizing this orthostatic intolerance is elicited by the associated central venous pressure response.

Shimizu, M.↗
NASA NTRS2020

Thoracic Pressure Does Not Impact CSF Pressure via Compartment Compliance

Space acquired neuro-ocular syndrome (SANS) remains a difficult risk to characterize due to the complex multi-factorial etiology related to physiological responses to the spaceflight environment. Fluid shift and the resultant change on the Cardiovascular (CV) and cerebral spinal fluid systems (CSF) in the absence of gravity continue to be considered a contributing factor to the progression of SANS. In this study, we utilize a computational model of the CSF and CV interface to establish the sensitivity that intracranial pressure, and subsequently the optic nerve sheath pressure, exhibits due to variations in thoracic pressure, assuming the cranial perfusion pressure, i.e. mean arterial pressure (MAP) to central venous pressure (CVP), is known. Methods: The GRC Cross cutting computational modeling project created as model of the CSF and CV interaction within the cranial vault by extending the work of Stevens et al. [1] by modifying the representative anatomy to include a separate venous sinus, jugular veins, secondary veins and extra jugular pathways [2-3] to more adequately represent the vascular drainage pathways from the cranial vault (Figure 1). Assuming the MAP, CVP and thoracic pressure are known, we initiated this enhanced computational model assuming a supine positon and utilized a linear ramp to vary the thoracic pressure from the assumed supine state to the target pressure corresponding to set MAP and CVP values. The model generates the time based CSF pressure values (Figure2). Results and Conclusions: Following this analysis, CSF pressure shows significant independence from thoracic pressure changes (16 mmHg in thoracic pressure produces < 1mmHg change in CSF pressure), being mostly dependent on perfusion pressure. Similarly fluid redistribution is not predicted to be impacted over a level of 1mL. We note that this simulation represents an acute changes (order of 10's of minutes) and does not represent the long term effects.

Munster, Drayton W.↗
NASA NTRS2000

Low LBNP tolerance in men is associated with attenuated activation of the renin-angiotensin system

Plasma vasoactive hormone concentrations [epinephrine (p(Epi)), norepinephrine (p(NE)), ANG II (p(ANG II)), vasopressin (p(VP)), endothelin-1 (p(ET-1))] and plasma renin activity (p(RA)) were measured periodically and compared during lower body negative pressure (LBNP) to test the hypothesis that responsiveness of the renin-angiotensin system, the latter being one of the most powerful vasoconstrictors in the body, is of major importance for LBNP tolerance. Healthy men on a controlled diet (2,822 cal/day, 2 mmol. kg(-1). day(-1) Na(+)) were exposed to 30 min of LBNP from -15 to -50 mmHg. LBNP was uneventful for seven men [25 +/- 2 yr, high-tolerance (HiTol) group], but eight men (26 +/- 3 yr) reached presyncope after 11 +/- 1 min [P < 0.001, low-tolerance (LoTol) group]. Mean arterial pressure (MAP) did not change measurably, but central venous pressure and left atrial diameter decreased similarly in both groups (5-6 mmHg, by approximately 30%, P < 0.05). Control (0 mmHg LBNP) hormone concentrations were similar between groups, however, p(RA) differed between them (LoTol 0.6 +/- 0.1, HiTol 1.2 +/- 0.1 ng ANG I. ml(-1). h(-1), P < 0.05). LBNP increased (P < 0. 05) p(RA) and p(ANG II), respectively, more in the HiTol group (9.9 +/- 2.2 ng ANG I. ml(-1). h(-1) and 58 +/- 12 pg/ml) than in LoTol subjects (4.3 +/- 0.9 ng ANG I. ml(-1). h(-1) and 28 +/- 6 pg/ml). In contrast, the increase in p(VP) was higher (P < 0.05) in the LoTol than in the HiTol group. The increases (P < 0.05) for p(NE) were nonsignificant between groups, and p(ET-1) remained unchanged. Thus there may be a causal relationship between attenuated activation of p(RA) and p(ANG II) and presyncope, with p(VP) being a possible cofactor. Measurement of resting p(RA) may be of predictive value for those with lower hypotensive tolerance.

NASA Center ARC↗
NASA NTRS1999

Potential Mechanism Leading to Impaired Thermoregulation Following Microgravity Exposure

Prolonged exposure to microgravity or its analogues impairs thermoregulation in humans evidenced by higher internal temperatures following the exposure during a thermal challenge. Although the mechanism leading to this response has not been clearly delineated, we identified that prolonged head-down tilt (HDT) markedly impairs thermoregulatory reflex control of skin blood flow, as demonstrated by an increased internal temperature threshold for cutaneous vasodilation, and by a reduced slope of the relationship between the elevation in skin blood flow relative to the elevation in internal temperature. Recently, Fortney et al. identified similar responses in two individuals following 115 days of microgravity exposure. One possible mechanism leading to altered cutaneous vasodilation during a thermal challenge following actual or simulated microgravity exposure may be associated with baroreflex-mediated attenuation in the elevation of skin blood flow. During a heat stress the elevation in skin blood flow is accomplished through a combination of increased cutaneous vascular conductance and cardiac output, both of which result in central venous pressure (CVP) decreasing 2-6 mmHg. Reductions in CVP of this magnitude in normothermia decrease muscle blood flow and skin blood flow presumably through unloading the cardiopulmonary baroreceptors. It is unclear whether the reduction in CVP, and accompanying cardiopulmonary baroreceptor unloading, during passive heating buffers the elevation in skin blood flow. That is, would the elevation in skin blood flow be greater if CVP did not decrease, or decreased to a lesser extent during the heat stress? Conversely, if CVP decreased to a greater extend during a thermal challenge following a perturbation such as prolonged HDT, would the elevation in skin blood flow be attenuated during that thermal challenge? Given that prolonged HDT decreases plasma volume and central venous pressure, such a finding would provide a plausible hypothesis to explain why skin blood flow does not increase to the same extent during a heat stress following simulated or actual microgravity exposure. Thus, the purpose of this project was to identify whether cardiopulmonary baroreceptor unloading coincident with heat stress buffers the elevation in skin blood flow.

Crandall, C. G.↗
NASA NTRS1994

Aortic baroreflex control of heart rate after 15 days of simulated microgravity exposure

To determine the effects of simulated microgravity on aortic baroreflex control of heart rate, we exposed seven male subjects to 15 days of bed rest in the 6 deg head-down position. The sensitivity of the aortic-cardiac baroreflex was determined during a steady-state phenylephrine-induced increase in mean arterial pressure combined with lower body negative pressure to counteract central venous pressure increases and neck pressure to offset the increased carotid sinus transmural pressure. The aortic-cardiac baroreflex gain was assessed by determining the ratio of the change in heart rate to the change in mean arterial pressure between baseline conditions and aortic baroreceptor-isolated conditions (i.e., phenylephrine + lower body negative pressure + neck pressure stage). Fifteen days of head-down tilt increased the gain of the aortic-cardiac baroreflex. Reductions in blood volume and/or maximal aerobic capacity may represent the underlying mechanism(s) responsible for increased aortic baroreflex responsiveness after exposure to a ground-based analogue of microgravity.

Crandall, Craig G.↗
NASA NTRS1999

Low LBNP Tolerance in Men is Associated With Attenuated Activation of Renin-Angiotensin System

Vasoactive hormone concentrations (epinephrine (pE), norepinephrine (pNE), angiotensin II (pATII), vasopressin (pVP), endothelin 1 (pET1)] and plasma renin activity (pRA) were measured during lower body negative pressure (LBNP) to test the hypothesis that responsiveness of the reninangiotensin system is related to LBNP tolerance. Healthy men (2,822 cal per day, 2 mmol per kilogram per day Na (+)) were exposed to 30 min of progressive LBNP to -50mmHg. LBNP was uneventful for 7 men (2512 yr, HiTol group), but 8 men (26 plus or minus 3 yr) reached pre-syncope after 11 plus or minus 1 min (P less than 0.001, LoTol group). Mean arterial pressure was unchanged. Central venous pressure and left atrial diameter decreased in both groups (5-6 mmHg by 30%, P less than 0.05). Control [hormone] were similar but, pRA differed between groups (LoTol 0.6 plus or minus 0.1, HiTol 1.2 plus or minus 0.1 ng Ang1 per milliliter per hour, per hour, P less than 0.05). LBNP increased (P less than 0.05) pRA and pATII more in HiTol (9.9 plus or minus 2.2 ng Ang1 per milliliter per hour and 58 plus or minus 12 pg per milliliter) than LoTol (4.3 plus or minus 0.9 ng Angl per milliliter per hour and 28 plus or minus 6 pg per milliliter). In contrast, pVP was higher (P less than 0.05) in LoTol than in HiTol. The response of the renin-angiotensin system seems linked to the occurrence of pre-syncope, and measurement of resting pRA may be predictive.

Greenleaf, John E.↗
NASA NTRS1999

Low LBNP Tolerance in Men is Associated With Attenuated Activation of The Renin-Angiotensin System

Vasoactive hormone concentrations [epinephrine (pE), norepinephrine (pNE), angiotensin II (pATII), vasopressin (pVP), endothelin 1 (pET1)] and plasma renin activity (pRA) were measured during lower body negative pressure (LBNP) to test the hypothesis that responsiveness of the renin-angiotensin system is related to LBNP tolerance. Healthy men (2,822 cal/day(exp -1), 2 mmol*kg(exp -1)*day(exp -1)) Na(+)) were exposed to 30 minutes of progressive LBNP to -50 mmHg. LBNP was uneventful for seven men (25 +/- 2 years, HiTol group), but eight men (26 +/- 3 years) reached pre-syncope after 11 +/- 1 minutes (P < 0.001, LoTol group). Mean arterial pressure was unchanged. Central venous pressure and left atrial diameter decreased in both groups (5-6 mmHg by approx. 30%, P < 0.05). Control [hormone] were similar but, pRA differed between groups (LoTol 0.6 +/- 0.1, HiTol 1.2 +/- 0.1 ng Ang1/(ml(exp -1)*h(exp -1)), P < 0.05). LBNP increased (P < 0.05) pRA and pATII more in HiTol (9.9 +/- 2.2 ng Ang1/(ml(exp -1)*h(exp -1)) and 58 +/- 12 pg/ml(exp -1)) than LoTol (4.3 +/- 0.9 ng Ang1/(ml*h) and 28 +/- 6 pg/ml(exp -1)). In contrast, pVP was higher (P < 0.05) in LoTol than in HiTol. The response of the renin-angiotensin system seems linked to the occurrence of pre-syncope, and measurement of resting pRA may be predictive.

Greenleaf, J. E.↗