Effects of passive heating on central blood volume and ventricular dimensions in humans

Mixed findings regarding the effects of whole-body heat stress on central blood volume have been reported. This study evaluated the hypothesis that heat stress reduces central blood volume and alters blood volume distribution. Ten healthy experimental and seven healthy time control (i.e. non-heat stressed) subjects participated in this protocol. Changes in regional blood volume during heat stress and time control were estimated using technetium-99m labelled autologous red blood cells and gamma camera imaging. Whole-body heating increased internal temperature (> 1.0 degrees C), cutaneous vascular conductance (approximately fivefold), and heart rate (52 +/- 2 to 93 +/- 4 beats min(-1)), while reducing central venous pressure (5.5 +/- 07 to 0.2 +/- 0.6 mmHg) accompanied by minor decreases in mean arterial pressure (all P < 0.05). The heat stress reduced the blood volume of the heart (18 +/- 2%), heart plus central vasculature (17 +/- 2%), thorax (14 +/- 2%), inferior vena cava (23 +/- 2%) and liver (23 +/- 2%) (all P 相似文献   

Vasopressin and renin responses to hemorrhage in conscious, cardiac-denervated dogs

We measured plasma arginine vasopressin (AVP) and plasma renin activity (PRA) during continuous hemorrhage in cardiac-denervated and sham-operated conscious dogs. Hemorrhage produced comparable decreases in aortic pressure, cardiac output, stroke volume, pulmonary arterial pressure, and left and right atrial pressures in each group of dogs. After 10 ml blood/kg body wt had been removed, AVP was increased in sham-operated dogs (P less than 0.05) but not in cardiac-denervated dogs. After 20 and 30 ml blood/kg body wt had been removed, AVP was increased in all dogs, but the response was markedly attenuated in cardiac-denervated dogs. Hemorrhage at 10 and 20 ml/kg caused comparable increases in PRA in each group of dogs. However, at 30 ml/kg hemorrhage the increase in PRA was significantly higher in cardiac-denervated dogs than in sham-operated dogs. Our results suggest that cardiac receptors play a dominant role in mediating the release of AVP during hemorrhage in conscious dogs. In contrast, we found no evidence for a dominant role of cardiac receptors in mediating renin secretion during hemorrhage.     

Effects of sympathetic inhibition on blood pressure and renal responses to central hypervolaemia in normal humans

The purpose of this study was to evaluate the effects of short-term sympathetic inhibition with clonidine on blood pressure and renal responses to central hypervolaemia induced by thermoneutral head-out water immersion. Eleven healthy subjects were randomly studied on two occasions, during a 1 h pre-immersion period, 2 h of water immersion and a 1 h post-immersion period, after either placebo or clonidine treatment. Clonidine caused a significant suppression of plasma adrenaline, plasma noradrenaline, urinary noradrenaline excretion and mean arterial blood pressure. Blood pressure remained constant during water immersion after both placebo and clonidine, compared with the respective pre-immersion control values. The suppression pattern of plasma catecholamines and urinary noradrenaline in response to water immersion during placebo was similar after clonidine treatment. Renal volume excretion was not affected by clonidine. In contrast, clonidine caused a significant attenuation of the immersion-induced stimulation of natriuresis (maximum -33±12%, P<0.01, compared with placebo). These data indicate that the renal capacity to excrete sodium is impaired during moderate blood pressure reduction by short-term sympathetic inhibition with clonidine, whereas the regulation of arterial blood pressure in response to central hypervolaemia is maintained.     

Increases in central blood volume modulate carotid baroreflex resetting during dynamic exercise in humans

We sought to determine if resetting of the carotid-vasomotor baroreflex function curve during exercise is modulated by changes in central blood volume (CBV). CBV was increased during exercise by altering: (1) subject posture (supine versus upright) and (2) pedal frequency (80 versus 60 revolutions min⁻¹ (r.p.m.)); while oxygen uptake (     ) was kept constant. Eight male subjects performed three exercise trials: upright cycling at 60 r.p.m. (control); supine cycling at 60 r.p.m. (SupEX) and upright cycling at 80 r.p.m. to enhance the muscle pump (80EX). During each condition, carotid baroreflex (CBR) function was determined using the rapid neck pressure (NP) and neck suction (NS) protocol. Although mean arterial pressure (MAP) was significantly elevated from rest (88 ± 2 mmHg) during all exercise conditions ( P < 0.001), the increase in MAP was lower during SupEX (94 ± 2 mmHg) and 80EX (95 ± 2 mmHg) compared with control (105 ± 2 mmHg, P < 0.05). Importantly, the blood pressure responses to NP and NS were maintained around these changed operating points of MAP. However, in comparison to control, the carotid-vasomotor baroreflex function curve was relocated downward and leftward when CBV was increased during SupEX and 80EX. These alterations in CBR resetting occurred without any differences in     or heart rate between the exercise conditions. Thus, increasing CBV and loading the cardiopulmonary baroreflex reduces the magnitude of exercise-induced increases in MAP and CBR resetting. These findings suggest that changes in cardiopulmonary baroreceptor load influence carotid baroreflex resetting during dynamic exercise.     

Arterial diameter during central volume depletion in humans

The luminal diameter of the radial artery was followed by high frequency ultrasound during 50° head-up tilt-induced central volume depletion in ten healthy subjects of whom six were tilted twice and pretreated with the serotonin receptor antagonist methysergide or placebo following a double-blind randomized design. Eight subjects without active treatment experienced presyncopal symptoms after 16–45 (mean 32 min). Central volume depletion was indicated by an increase in mean thoracic electrical impedance [from 31.5 (SEM 1.6) to 33.4 (SEM 1.7) P < 0.05]. Cardiac output decreased [from 4.1 (SEM 0.3) to 2.2 (SEM 0.3) l · min^–1] and heart rate [HR, from 64 (SEM 3) to 100 (SEM 7) beats · min^–1], mean arterial pressure {MAP, from 77 (SEM 4) to 89 (SEM 2) mmHg [10.3 (SEM 0.53 to 11.9 (SEM 0.27) kPa]} and total peripheral resistance {TPR, from 19 (SEM 2) to 34 (SEM 4) mmHg · min · l^–] [2.5 (SEM 0.27) to 4.5 (SEM 0.53) kPa · min^–1]} increased; but with the appearance of presyncopal symptoms, HR, MAP and TPR were reduced to 65 (SEM 8) beats · min^–1, 46 (SEM 4) mmHg [6.1(SEM 0.53) kPa] and 18 (SEM 3) mmHg · min · l^–1 [2.4 (SEM 0.4) kPa · min^–1 · l^–], respectively (P < 0.05). Vascular resistance was reflected in the arterial diameter which decreased from 2.42 (SEM 0.17) to 2.27 (SEM 0.14) mm during head-up tilt and increased to 2.71 (SEM 0.14) mm with the appearance of presyncopal symptoms (P < 0.05). Methysergide reduced the resting radial (15 ± 2%) and temporal artery diameters (10 ± 3%) (P < 0.05); however, it affected neither tilt-tolerance nor the central cardiovascular response to tilt. The results suggested a serotonergic influence on arterial tone at rest, and demonstrated that vessels as large as the radial artery participated in vascular control during central volume depletion independent of such a serotonergic influence.     

Haemodynamic responses to nonhypotensive central hypovolaemia induced by lower body negative pressure in men and women

Summary Haemodynamic responses to low levels of lower body negative pressure (LBNP) were investigated in two groups of healthy, normotensive volunteers (8 men and 8 women) during two repeated experimental runs on two occasions, the latter determined by the different phases of the menstrual cycle in the women. The data consisted of systolic blood pressure (SBP), diastolic blood pressure (DBP) and mean blood pressure (MBP), pulse rate (f _c), forearm blood flow (FBF) and forearm vascular conductance (FC). The resting cardiovascular status was similar in men and women, except that women had a significantly higher f _c than men. LBNP (1.3, 2.7 and 4 kPa) had no significant effect on any BP variable or on f _c. However, FBF and FC were reduced at all levels of LBNP. Significant overshoots in FBF and FC were seen in all subjects following the release of LBNP of 2.7 and 4 kPa and, in most cases, after release of LBNP of 1.3 kPa. There were no significant gender differences in any of the responses to LBNP. Furthermore, none of the cardiovascular variables measured showed significant differences between the follicular and luteal phases of the menstrual cycle in women, either at rest or during exposure to LBNP, and the responses in the men on the two occasions were not different. These findings indicate that gender differences in responses to LBNP hypothesized previously are not apparent during and after exposure to low levels of LBNP.     

Renal response to central volume expansion in humans is attenuated at night

The renal response to central volume expansion induced by head-out water immersion was examined in 10 normal, salt-replete subjects studied during the day (0900-1300) and during the night (0000-0400). Sodium excretion in the hour preceding the study was 155 +/- 21 mueq/min and 120 +/- 14 mueq/min, respectively. During the day, immersion was followed by a natriuresis, which reached a mean peak level of 293 +/- 46 mueq/min during the 2nd h of immersion and which was maintained for the remainder of the immersion. During the night, there was no significant increase in sodium excretion from prestudy values during the first 3 h of immersion. Values rose significantly in the 4th h and reached a mean peak level of 211 +/- 20 mueq/min. Potassium excretion rose during the day (from 61 +/- 12 mueq/min to 126 +/- 16 mueq/min) but was unaltered at night. Neither glomerular filtration rate nor plasma levels of aldosterone differed between day and night. To exclude the possibility that the blunted nocturnal natriuresis could be explained by a lesser degree of central fluid translocation induced by immersion at night six normal salt-replete subjects received a 2-liter infusion of normal saline administered over 4 h during the day and during the night. The blunting of the nocturnal natriuresis was again observed. We conclude that, in addition to well-described diurnal variations in electrolyte excretion, there are diurnal variations in the responsivity of volume regulatory mechanisms.     

Hemodynamic responses to acute hematocrit and blood volume alterations in rats

Previous investigations of polycythemia in rodents failed to delineate the effects of the increased hematocrits from the effects of possible changes in blood volume. The hemodynamic responses of anesthetized rats to acutely produced increases in hematocrit and blood volume were therefore studied in this experiment. Acute isovolumetric polycythemia decreased O₂ transport from a control value of 44.9 to 35.1 ml/min/kg 60 min after the exchange-transfusion. However, the high venous O₂ content (over 12 Vol.-%) following the production of isovolumetric polycythemia suggested that there was still sufficient oxygen available to the tissues. Hypervolemia significantly modified the response to acute polycythemia. When hematocrit was maintained at a constant level, acute hypervolemia increased O₂ transport (to 54.6 ml/min/kg after 60 min), and when acute hypervolemia and polycythemia were induced simultaneously, O₂ transport was transiently increased (to 57.5 ml/min/kg after 15 min) and then returned to a value similar to the control level. This work was supported in part by Air Force Office of Scientific Research, Air Force Systems Command, Grant AFOSR 73-2455     

Cerebral oxygenation and blood volume responses to seated whole-body vibration

Role of backrest support and hand grip contractions on regional cerebral oxygenation and blood volume were evaluated by near infrared spectroscopy in 13 healthy men during whole-body vibration (WBV). Subjects were exposed to three WBV (3, 4.5, and 6 Hz at ∼0.9 g_rms in the vertical direction), in a randomized order on separate days. During WBV, subjects performed right-hand maximal voluntary intermittent rhythmic hand grip contractions for 1 min. Subjects demonstrated highest oxygenation and blood volume values at 4.5 Hz, however, these responses were similar with and without backrest support (P>0.01). Compared to WBV alone, addition of hand grip exercise during WBV further increased oxygenation (0.07±0.11 vs. 0.004±0.11 od, P=0.003) and blood volume (0.156±0.20 vs. 0.066±0.17 od, P=0.000) in the right forehead. Peak oxygen uptake did not correlate to changes in oxygenation and blood volume (P>0.01). Based on the increase in ventilation volume and no change in the ratio of ventilation volume and expired carbon dioxide (P>0.01), it is concluded that WBV induces hyperventilation that might activate the pre-frontal cortical region, thus influencing cerebral responses through neuronal activation.     

Vasoconstriction and blood flow responses in visceral arteries to mental task in humans

The vascular responses to mental task in visceral arteries in humans have not been elucidated. We observed the responses in the renal (RA) and superior mesenteric (SMA) arteries to mental stress, using simultaneous pulsed and echo Doppler ultrasound flowmetry. Nine healthy females performed a computerized colour word conflict test (CWT) for 3 min. The mean blood velocity (MBV) in the right RA and SMA, heart rate (HR) and blood pressure were measured. The mean arterial pressure (MAP) was divided by the flow velocity to assess the vascular resistance (VR). The CWT significantly increased the MAP, HR and VR in both arteries from the first minute. During the CWT, flow in the RA decreased significantly at the third minute relative to baseline, while flow in the SMA showed no significant change from the first to the third minute. The degree of vasoconstriction in the RA bed was greater than that in the SMA bed. These results suggest that the mental task causes vasoconstriction in visceral arteries, and imply that it induces differential blood flow and vascular responses in visceral arteries.     

Haemodynamic responses to dehydration in the resting and exercising human leg

Dehydration and hyperthermia reduces leg blood flow (LBF), cardiac output ( $ \dot{Q} $ ) and arterial pressure during whole-body exercise. It is unknown whether the reductions in blood flow are associated with dehydration-induced alterations in arterial blood oxygen content (C _aO₂) and O₂-dependent signalling. This study investigated the impact of dehydration and concomitant alterations in C _aO₂ upon LBF and $ \dot{Q} $ . Haemodynamics, arterial and femoral venous blood parameters and plasma [ATP] were measured at rest and during one-legged knee-extensor exercise in 7 males in four conditions: (1) control, (2) mild dehydration, (3) moderate dehydration, and (4) rehydration. Relative to control, C _aO₂ and LBF increased with dehydration at rest and during exercise (C _aO₂: from 199 ± 1 to 208 ± 2, and 202 ± 2 to 210 ± 2 ml L^?1 and LBF: from 0.38 ± 0.04 to 0.77 ± 0.09, and 1.64 ± 0.09 to 1.88 ± 0.1 L min^?1, respectively). Similarly, $ \dot{Q} $ was unchanged or increased with dehydration at rest and during exercise, whereas arterial and leg perfusion pressures declined. Following rehydration, C _aO₂ declined (to 193 ± 2 mL L^?1) but LBF remained elevated. Alterations in LBF were unrelated to C _aO₂ (r ² = 0.13–0.27, P = 0.48–0.64) and plasma [ATP]. These findings suggest dehydration and concomitant alterations in C _aO₂ do not compromise LBF despite reductions in plasma [ATP]. While an additive or synergistic effect cannot be excluded, reductions in LBF during exercise with dehydration may not necessarily be associated with alterations in C _aO₂ and/or intravascular [ATP].     

Haemodynamic and humoral responses to repeated hypotensive haemorrhage in conscious sheep

Haemodynamic and humoral responses to two subsequent hypotensive haemorrhages, separated by 3 hours and each followed by retransfusion, were studied in unanaesthetized sheep. Haemorrhage was induced by removal of blood from a jugular vein at a rate of 0.7 ml kg-1 min-1 until the mean systemic arterial pressure suddenly decreased by 35 mmHg or more. In addition to the mean systemic arterial pressure, the cardiac output, the mean pulmonary arterial pressure, the central venous pressure and the pulmonary capillary wedge pressure decreased in response to each haemorrhage. The recovery of the systemic and pulmonary arterial pressure was slower and/or less efficient after the second haemorrhage, due to a less pronounced increase of the vascular resistance. Relative bradycardia, in association with the abrupt fall of the mean systemic arterial pressure, was more apparent during the first haemorrhage. The plasma levels of vasopressin, renin activity and angiotensin II were increased by each blood removal, but the vasopressin response to the second haemorrhage was significantly reduced. The plasma noradrenaline concentration was slightly and transiently elevated only in response to the second haemorrhage. The concentration of neuropeptide Y-like immunoreactivity in plasma was unaffected by both haemorrhages. It is suggested that the reduced and delayed increase in the systemic vascular resistance, accompanied by impaired recovery of the arterial pressure, and the relative absence of 'bleeding bradycardia', during the second haemorrhage, were due to the diminished vasopressin response.     

Cardiovascular responses to heat stress and blood volume displacements during exercise in man

Summary Subjects exercised in the upright position at approximately 50% of maximal oxygen consumption in four situations: in 25 C air, in 45 C air [mean skin temperature ( _sk) 35 C], in 35 C water immersed to the level of the xiphoid process, and finally wearing a suit perfused with 35 C water. The water immersion prevented gravitational shifts of blood volume to the legs. In this situation the forearm blood flow (FBF) rose continually with increasing core temperature (T_es) in contrast to the attenuation in rise above 38 C T_es in 45 C air. The differences were significant above 38.6 C T_es in experiments in eight subjects. The effects of immersion on cardiac output (CO), stroke volume (SV), and heart rate (HR) were studied in five of the subjects in relation to T_es, since the rate of rise of T_es was different in the four situations. CO and SV tended to be higher during both rest and exercise in the water than in the other three conditions, while HR rose in the same manner with increasing core temperature, except that it was lower in 25 C air, where T_es was lower. Thus, the prevention of hydrostatic shifts of peripheral venous volume permitted the maintenance of a higher SV and peripheral blood flow, and enhanced the ability of the circulation to deal with the combined exercise and heat stress.Supported by the Danish Space Board (1112-32/81), the Danish Medical Research Council (512–15983), and the Danish Sports Research Council. Dr. Rowell was supported in part by NHLBI Grant HL 16910     

Haemodynamic and hormonal responses to heat exposure in a Finnish sauna bath

Summary Eight healthy young men were studied during three periods of heat exposure in a Finnish sauna bath: at 80° C dry bulb (80 D) and 100° C dry bulb (100 D) temperatures until subjective discomfort, and in 80° C dry heat, becoming humid (80 DH) until subjective exhaustion. Oral temperature increased 1.1° C at 80 D, 1.9° C at 100 D and 3.2° C at 80 DH. Heart rate increased about 60% at 80 D, 90% at 100 D and 130% at 80 DH. Plasma noradrenaline increased about 100% at 80 D, 160% at 100 D and 310% at 80 DH. Adrenaline did not change. Plasma prolactin increased 2-fold at 80 D, 7-fold at 100 D and 10-fold at 80 DH. Blood concentrations of the beta-endorphin immunoreactivity at 100 D, adrenocorticotropic hormone (ACTH) at 100 D and 80 DH, growth hormone at 100 D and testosterone at 80 DH also increased, but cortisol at 80 D and 100 D decreased. The plasma prostaglandin E₂ and serum thromboxane B₂ levels did not change. Patterns related to heat exposure were observed for heart rate, plasma noradrenaline, ACTH and prolactin in the three study periods.