Increase In Central Blood Volume Research Articles

Human cardiovascular responses to passive heat stress

Humans, like other tropical animals, can tolerate high levels of heat stress (albeit for short periods of time) provided that (1) they avoid contact with extremely hot surfaces, (2) they can produce and evaporate sufficient sweat, and (3) the cardiovascular system that supports homeostasis under such conditions is not compromised. Indeed, during episodic severe heat waves that result in increased death rates especially among the elderly, cardiovascular disease is the primary or contributing cause of death in > 80% of examined cases (Smenza et al. 1996). Crandall et al. (2008) point out in this issue of The Journal of Physiology that ‘whole-body heating has the potential to cause significant cardiovascular stress that … may be second only to [that] associated with exercise’. Because of the high compliance of the cutaneous circulation and the lack of muscle pump function during severe and prolonged passive heating, the strain on the left ventricle – which provides all of the energy to essentially double cardiac output under such conditions – may be even greater than that seen during exercise. The response of the cardiovascular system to passive heat stress is an elegant example of homeostatic regulation and integration, worthy of being taught in every physiology class. In the classic experimental model of passive whole-body heating, skin temperature is elevated and clamped using water-perfused suits and core temperature rises as heat is transferred internally by convection and conduction. Cutaneous blood flow increases remarkably from basal values of 200 ml min−1 to upwards of 8 l min−1, yet arterial pressure is well maintained by a doubling of cardiac output (due to an increase in heart rate and maintenance of, or a slight elevation in, stroke volume despite falling central venous pressure) coupled with a redistribution of flow from renal and splanchnic vascular beds (Rowell et al. 1969). Elderly subjects, even those with no apparent cardiac dysfunction, respond to passive heating with an attenuated rise in skin blood flow coupled with both a lower cardiac output response and a diminished ability to redistribute flow from splanchnic and renal circulations, relying on a greater portion of their chronotropic reserve to compensate for a reduced inotropic response (Minson et al. 1998). A compromised left ventricle, e.g. due to heart disease or advanced ageing, may not be capable of meeting these demands in light of the requisite increase in cardiac work (i.e. the area of the flow–volume loop). While flow characteristics of the integrated cardiovascular response to heating are well understood, some controversy has existed about capacitance characteristics of the response. Muller (1905) first hypothesized a reduction in central blood volume (CBV) during passive heating, yet Rowell et al. (1969) noted a slight increase in CBV which he later described as a ‘pre-ventricular sump’ phenomenon. Crandall et al. (2008) approached this question using γ camera imaging of 99mTc-labelled autologous red blood cells. Their results demonstrated that thoracic blood volume, an index of CBV, was indeed decreased during supine passive heating. Further, blood volume was reduced in splanchnic circulations. These two findings support the hypothesized shift of blood volume from the central circulation to the skin to sustain heat dissipation. A second important finding from Crandall and colleagues (2008) is the 13% increase in left ventricular ejection fraction (EF) that occurs in concert with the elevation in heart rate in young heated subjects. The fact that stroke volume does not fall (and may increase slightly) despite falling central venous pressure presents a strong argument for increased cardiac contractility. While the authors concede that EF is an imperfect index of contractility, the link between the two is particularly robust under conditions of supine heating. In combination with the data of Rowell and Minson, the preponderance of cardiovascular morbidity and mortality (e.g. Smenza et al. 1996) during heat waves – the most closely related natural occurrence of sustained passive heating – is predictable. It is important to note that the subjects in this meritorious investigation were young, healthy and medication free. Given the preponderance of heat-related problems in the elderly and the otherwise cardiovascularly compromised, it remains uncertain whether their attenuated flow responses (Minson et al. 1998) are balanced by disparate volume characteristics. However, the present contribution of Crandall et al. lends additional support to the hypothesis that a large number of heat-related deaths among the elderly during heat waves may be attributable to increased strain on an already compromised left ventricle.

Reduced central blood volume and cardiac output and increased vascular resistance during static handgrip exercise in postural tachycardia syndrome

Postural tachycardia syndrome (POTS) is characterized by exercise intolerance and sympathoactivation. To examine whether abnormal cardiac output and central blood volume changes occur during exercise in POTS, we studied 29 patients with POTS (17-29 yr) and 12 healthy subjects (18-27 yr) using impedance and venous occlusion plethysmography to assess regional blood volumes and flows during supine static handgrip to evoke the exercise pressor reflex. POTS was subgrouped into normal and low-flow groups based on calf blood flow. We examined autonomic effects with variability techniques. During handgrip, systolic blood pressure increased from 112 +/- 4 to 139 +/- 9 mmHg in control, from 119 +/- 6 to 143 +/- 9 in normal-flow POTS, but only from 117 +/- 4 to 128 +/- 6 in low-flow POTS. Heart rate increased from 63 +/- 6 to 82 +/- 4 beats/min in control, 76 +/- 3 to 92 +/- 6 beats/min in normal-flow POTS, and 88 +/- 4 to 100 +/- 6 beats/min in low-flow POTS. Heart rate variability and coherence markedly decreased in low-flow POTS, indicating uncoupling of baroreflex heart rate regulation. The increase in central blood volume with handgrip was absent in low-flow POTS and blunted in normal-flow POTS associated with abnormal splanchnic emptying. Cardiac output increased in control, was unchanged in low-flow POTS, and was attenuated in normal-flow POTS. Total peripheral resistance was increased compared with control in all POTS. The exercise pressor reflex was attenuated in low-flow POTS. While increased cardiac output and central blood volume characterizes controls, increased peripheral resistance with blunted or eliminated in central blood volume increments characterizes POTS and may contribute to exercise intolerance.

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.

Increases In Central Blood Volume Modulate Carotid Baroreflex Resetting During Dynamic Exercise In Humans

Increases In Central Blood Volume Modulate Carotid Baroreflex Resetting During Dynamic Exercise In Humans

The Effect Of Nacl Ingestion On Plasma Osmolality And Thirst Ratings During Cold Exposure

PURPOSE: Cold exposure has previously been shown to attenuate thirst perception in hyperosmotic hypovolemic subjects, likely through an increase in central volume. This study attempted to override this volume-mediated thirst attenuation by further raising plasma osmolality in dehydrated subjects resting and exercising in the cold. METHODS: On four occasions, 8 males, age, 24.1 ± 5.5 yrs; height, 179.6 ± 10.5 cm; weight, 78.0 ± 13.4 kg; VO2max, 56.1 ± 5.9 ml·kg-1·min-1; % body fat, 9.9 ± 2.4%; and BMI, 23.9 ± 2.2 kg·m-2, performed a 90 minute exercise-dehydration protocol in 37°C to establish a 3.5-4% reduction in body weight. Subjects restricted fluid intake overnight, and the next morning were given either a drink containing NaCl (0.1 g of NaCl·kg-1 body weight in 500ml of H2O or Placebo (Kool-Aid in 500mL of H2O). Immediately following each treatment, subjects stood for 30 min at 24°C (equilibration). They then entered an environmental chamber set at Tair of 4°C where they stood for 45 min and then walked for 45 min at 60% VO2max. Blood samples were obtained pre-treatment, following equilibration at 24°C, and following rest and exercise at 4°C. RESULTS: On the morning of experimental testing, subjects were hyperosmotic and hypovolemic, verified by a 3.5-4% decrease in body weight and Posm of∼295 mmol·kg-1 H2O. Ratings of thirst perception were ∼6.7 (Very thirsty) before each drink (NaCl or Placebo). Compared to pre-drink ratings, cold exposure resulted in a decline (p<0.05) in thirst ratings in the Placebo trial, despite an elevated Posm (∼297.0 mmol·kg-1 H2O). The NaCl drink increased (p<0.05) Posm, in both the 24°C and 4°C environments vs. the Placebo trial. Thirst ratings for the NaCl drink were greater (p<0.05) in 23°C, and after rest and exercise in 4°C, compared to Placebo. CONCLUSIONS: The NaCl drink resulted in a further elevation of Posm in both environmental temperatures with a concomitant increase in thirst. As previously reported, cold reduces thirst sensations regardless of elevated Posm, likely resulting from an increase in central blood volume and stimulation of central volume receptors. However, these results suggest that the attenuation of thirst associated with cold exposure may be over-ridden by the further elevating Posm with NaCl ingestion.

Changes in regional blood volume and blood flow during static handgrip

Increased blood pressure (BP) and heart rate during exercise characterizes the exercise pressor reflex. When evoked by static handgrip, mechanoreceptors and metaboreceptors produce regional changes in blood volume and blood flow, which are incompletely characterized in humans. We studied 16 healthy subjects aged 20-27 yr using segmental impedance plethysmography validated against dye dilution and venous occlusion plethysmography to noninvasively measure changes in regional blood volumes and blood flows. Static handgrip while in supine position was performed for 2 min without postexercise ischemia. Measurements of heart rate and BP variability and coherence analyses were used to examine baroreflex-mediated autonomic effects. During handgrip exercise, systolic BP increased from 120 +/- 10 to 148 +/- 14 mmHg, whereas heart rate increased from 60 +/- 8 to 82 +/- 12 beats/min. Heart rate variability decreased, whereas BP variability increased, and transfer function amplitude was reduced from 18 +/- 2 to 8 +/- 2 ms/mmHg at low frequencies of approximately 0.1 Hz. This was associated with marked reduction of coherence between BP and heart rate (from 0.76 +/- 0.10 to 0.26 +/- 0.05) indicative of uncoupling of heart rate regulation by the baroreflex. Cardiac output increased by approximately 18% with a 4.5% increase in central blood volume and an 8.5% increase in total peripheral resistance, suggesting increased cardiac preload and contractility. Splanchnic blood volume decreased reciprocally with smaller decreases in pelvic and leg volumes, increased splanchnic, pelvic and calf peripheral resistance, and evidence for splanchnic venoconstriction. We conclude that the exercise pressor reflex is associated with reduced baroreflex cardiovagal regulation and driven by increased cardiac output related to enhanced preload, cardiac contractility, and splanchnic blood mobilization.

Thirst Sensations and AVP Responses at Rest and during Exercise-Cold Exposure

The purpose of this study was to 1) determine the effect of hypohydration (HYPO) on thirst sensations during moderate exercise in the cold and 2) determine a possible mechanism for a cold-induced decline in thirst. In the first phase of the study, eight males walked on four occasions, in T-shirts, shorts, and shoes, at 50% VO2max, for 60 min in either a 4 degrees C (cold) or 27 degrees C (temperate) environment in a state of HYPO or euhydration (EU). In the second phase, nine males in states of EU or HYPO randomly performed four trials consisting of 30 min standing at 27 degrees C, followed by 30 min of standing and 30 min of treadmill exercise at 50% of VO2max, in either 4 degrees C or 27 degrees C air. In phase 1, thirst sensations were lower throughout 60 min of exercise (P < 0.05) in both HYPO and EU conditions during the cold trials. In phase 2, despite elevated plasma osmolality (P < 0.05), perception of thirst and plasma arginine vasopressin [AVP] similarly decreased (P < 0.05) after 30-min standing rest and 30-min exercise in the HYPO-cold trial, compared with the HYPO-temperate, EU-cold, and EU-temperate trials. When either euhydrated or hypohydrated, cold exposure attenuated thirst by up to 40% at rest and during moderate-intensity exercise. The attenuated thirst when hypohydrated during cold exposure was associated with lower plasma [AVP] despite an elevated plasma osmolality. This decline in thirst and AVP in the cold may be the result of peripheral vasoconstriction, mediating an increase in central blood volume and stimulation of central volume receptors.

Plasma volume expansion by albumin in cirrhosis. Relation to blood volume distribution, arterial compliance and severity of disease

Background/Aims: The aim of the study was to investigate the effect of a standard albumin load on blood volume distribution, arterial compliance, and the renin-angiotensin-aldosterone system in patients with different degrees of cirrhosis. Methods: 31 patients with cirrhosis (Child classes A/B/C=8/14/9) received an intravenous infusion of 40 g human serum albumin during a haemodynamic investigation. Results: Whereas plasma- and blood volume increased by 23 and 15%, respectively ( P<0.001), a significant increase in central blood volume was found only in class A patients (+8%, P<0.05), but not in class B or class C patients (+2.7%, not significant (n.s.)). In contrast, arterial compliance only increased significantly in class C patients (+18%, P<0.05), but not in class A or class B patients (+6%, n.s.). Plasma renin activity (PRA) decreased significantly in class C patients (−31%, P<0.05). When all patients were compared, the change in arterial compliance was inversely correlated to the change in PRA ( r=−0.50, P<0.01). Conclusions: Although infusion of albumin does not expand the central blood volume in patients with advanced cirrhosis, the results indicate a significant improvement in the low effective arterial blood volume of such patients, which may be important in the prevention of circulatory dysfunction.

Sodium homeostasis with chronic sodium loading in preascitic cirrhosis

BACKGROUNDPreascitic cirrhotic patients receiving 200 mmol of sodium daily for seven days remain in positive sodium balance. Thereafter, sodium handling is unknown.AIMTo assess renal sodium handling in preascitic cirrhosis on...

Pneumoperitoneum in healthy humans does not affect central blood volume or cardiac output.

This study addresses the question of whether the elevation of the mean arterial pressure and central venous pressure in response to pneumoperitoneum for laparoscopic surgery is caused by increases in central blood volume and/or cardiac output. Eleven patients in good cardiopulmonary health and scheduled for laparoscopic cholecystectomy, with a mean age of 42 years, were included. After induction of anaesthesia with fentanyl and propofol, radial arterial and central venous lines were introduced. The central blood volume and cardiac output were determined by the indicator-dilution technique, using inline densitometric measurements of indocyanine green (ICG). The measurements were made before and after the establishment of pneumoperitoneum by insufflation of carbon dioxide to an intra-abdominal pressure level of 11-13 mmHg. The mean arterial pressure (62+/-6 mmHg) increased after induction of pneumoperitoneum by 40+/-26% (P<0.05) and the central venous pressure increased from 6+/-4 mmHg to 8+/-6 mmHg (P<0.05). The cardiac output (4.3+/-0.9 L/min) and central blood volume (1.5+/-0.5 L) were not affected by the induction of pneumoperitoneum. In healthy anaesthetized subjects, the elevation of mean arterial pressure and central venous pressure in response to pneumoperitoneum was not caused by enhancement in cardiac output or central blood volume.

Acute Pulmonary Edema Associated With Placement of Waist-High, Custom-Fit Compression Stockings

Compression stockings are a safe, noninvasive treatment for patients with symptomatic orthostatic hypotension due to autonomic nervous system dysfunction. In this report, we describe a 75-year-old man who had development of pulmonary edema approximately 45 minutes after placement of compression stockings on the first postoperative day following a carotid endarterectomy. No sudden changes were noted on an electrocardiogram or echocardiogram or in the cardiac isoenzymes associated with the pulmonary edema. The patient had a history of coronary artery disease, diabetes mellitus-induced autonomic nervous system dysfunction, and recent surgery near the carotid baroreceptor. All these factors may have limited his ability to compensate for a rapid increase in central blood volume. The temporal relationship of the patient's respiratory distress to the placement of the compression stockings, in the absence of laboratory findings of primary cardiac dysfunction, make stocking-related fluid shift the likely precipitating event in the formation of acute pulmonary edema. This case suggests that compression stockings should be used with caution in patients with limited cardiac reserve.

Water exercise in pregnancy

Exercise in the water offers several physiological advantages to the pregnant woman. The hydrostatic force of water pushes extravascular fluid into the vascular spaces, producing an increase in central blood volume that may lead to increased uterine blood flow. This force is proportional to the depth of immersion. The increase in blood volume is proportional to the woman's edema. A marked diuresis and natriuresis accompanies the fluid shifts. The buoyancy of water supports the pregnant women. Water is thermoregulating. Studies of pregnant women exercising in the water have shown less fetal heart rate changes in the water than on land in response to exertion. Pregnant women's heart rates and blood pressures during water exercise are lower than on land exercise, reflecting the immersion-induced increase in circulating blood volume. The physiology of water exercise offers some compensation for the physiological changes of exercise on land that may beneficially affect pregnancy.

The kidney and essential hypertension: a link to osteoporosis?

Abnormalities of calcium metabolism independent of changes in intracellular calcium have been described in patients with essential hypertension. These include increased urinary calcium excretion for a given salt intake, a raised parathyroid hormone level, an increase in urinary cyclic AMP, a tendency for a low serum ionized calcium level, a raised 1,25-dihydroxyvitamin D level and an increased intestinal calcium reabsorption. These changes have been seen as a consequence of a primary renal calcium leak. We propose that these changes are secondary to a genetic defect in the ability of the kidney to excrete sodium. On the high salt intake in most Western countries (i.e. approximately 170 mmol/day sodium) compensatory mechanisms occur to try to overcome this defect. These compensatory mechanisms are responsible for the rise in blood pressure, but also cause an increase in central blood volume which is the direct cause of the increase in urinary calcium excretion. This causes a slightly negative calcium balance, and the other abnormalities of calcium metabolism can then be seen as a compensatory response to try to restore calcium balance to normal. This hypothesis explains the increase in kidney stones in essential hypertension and predicts that hypertensives, in the long term, will be more likely to develop bone demineralization (osteoporosis), as has been demonstrated in some animal models of hypertension. Increases in salt intake will not only cause a further rise in blood pressure, but will also increase urinary calcium excretion and aggravate the other abnormalities. A moderate reduction in salt intake from 170 to 70 mmol/day will lower the blood pressure and will tend to correct the abnormalities of calcium metabolism. It should simultaneously reduce the incidence of renal stones and the long-term risk of bone demineralization.

Effects of Periodic Obstructive Apneas on Venous Return in Closed-chest Dogs

With sleep apnea syndrome, mean cardiac output (CO) may fall. This implies a fall in venous return (VR) that is equal to the product of the pressure gradient for VR (GVR)--mean circulatory pressure (MCP)--right ventricular end-diastolic pressure and the conductance for VR (Gv). During airway obstruction there could also be shifts of blood volume between central and peripheral circulatory compartments. We studied these parameters in anesthetized closed-chest, spontaneously breathing dogs when hypoxia occurred (room air [RA] breathing) and when hypoxia was prevented (100% O2 breathing). Obstructive apneas were induced by completely occluding the endotracheal tube at end expiration for 1 min and allowing 1 min of spontaneous ventilation. During RA apneas, arterial PO2 decreased to 32.7 +/- 6.1 mm Hg (p < 0.01). Apnea reduced respiratory effort rate by 22.0 to 37.0% and was associated with inspiratory airway pressure swings in both RA and O2 of approximately -16.0 mm Hg. During apnea, on RA and O2 heart rate and mean arterial pressure decreased by 20 to 30 beats/min and by 8 to 12 mm Hg, respectively. On RA, CO decreased by 7.0% (not significant). In contrast, on O2, CO increased by 21.0% (p < 0.01). With RA apneas, GVR and MCP increased by 55% (p < 0.05) and Gv decreased by 63% (p < 0.05). On O2, there were no changes in GVR or Gv, and changes in CO were predictable from the baseline VR curve. With O2 there was an increase in central blood volume by 21.0% (p < 0.01) during the apneic phase.(ABSTRACT TRUNCATED AT 250 WORDS)

Pulmonary angiotensin-converting enzyme substrate hydrolysis during exercise.

We examined exercise-induced changes in indicator-dilution estimates of the angiotensin-converting enzyme first-order kinetic parameter, the ratio of a normalized maximal enzymatic conversion rate to the Michaelis constant (Amax/Km), which, under stable enzymatic conditions, will vary with the pulmonary vascular surface area accessible to vascular substrate, the extravascular lung water (an index of the proportion of lung tissue perfused), and the central blood volume (from pulmonary trunk to aorta). Experiments were performed in 10 mongrel dogs at rest and through two increasing levels of treadmill exercise, with the use of two vascular space tracers (labeled erythrocytes and albumin), a water space tracer ([1,8-14C]-octanediol), and a vascular endothelium surface area marker, benzoyl-Phe-Gly-Pro ([3H]BPGP), which is a pharmacologically inactive angiotensin-converting enzyme substrate. The exercise-induced increase in cardiac output was accompanied by a linear increase in central blood volume, and dilutional extravascular lung water rapidly increased to an asymptotic proportion close to 100% of postmortem vascular lung water. There was an average 55% [3H]BPGP hydrolysis, which did not vary with flow, and the computed Amax/Km increased linearly with exercise. We conclude that exercise results in complete lung tissue recruitment and increases the pulmonary vascular surface area available for BPGP hydrolysis linearly with flow, so that pulmonary vascular recruitment continues after full tissue recruitment.

Fluid-regulating hormones during exercise when central blood volume is increased by water immersion.

To examine the influence of an increase in central blood volume with head-out water immersion (WI) on fluid-regulating hormones during exercise, 10 healthy men underwent upright leg cycle exercise on land and with WI. Venous plasma renin activity and plasma venous concentrations of atrial natriuretic peptide, plasma aldosterone, and arginine vasopressin were determined at exercise intensities corresponding to approximately 40, 60, 80, and 100% peak oxygen consumption (VO2) and at minutes 1 and 5 of seated rest recovery within each environment. Peak VO2 did not differ on land and with WI. Atrial natriuretic peptide concentration was higher (P less than 0.05) and plasma renin activity was lower (P less than 0.05) in water than on land at 40% peak VO2 through minute 5 of recovery. Plasma aldosterone and arginine vasopressin concentrations were lower (P less than 0.05) in water at peak exercise and at minutes 1 and 5 of recovery. Osmolality and plasma sodium and potassium concentrations during exercise were similar in water and on land. The results indicate that WI alters the circulating levels of several hormones involved in fluid and electrolyte regulation during exercise. These hormonal alterations can best be explained by stimulation of low-pressure baroreceptors and atrial stretch due to increased central blood volume with head-out WI.

Plasma Concentrations of Atrial Natriuretic Factor and Hemodynamics in Pregnancy-Induced Hypertension

Plasma values of atrial natriuretic factor (ANF) were evaluated in 31 women with pregnancy-induced hypertension (PIH) and 31 normal pregnant women at the same age of gestation. In 27 women with PIH and 27 normal pregnant women forearm venous tone (FVT) was evaluated by Strain Gauge Plethysmography. Forearm vascular resistance (FVR) was measured as the ratio of mean blood pressure (MBP) to forearm blood flow. In addition Cardiac Index (CI) by means of transthoracic electrical bioimpedance and total peripheral vascular resistance (TPR) (with the Frank Equation) were also measured. In comparison with the normal pregnant women, the women with PIH had similar values of hematocrit (as an index of plasma volume) and significantly higher levels of FVR and TPR, while ANF plasma values did not differ significantly. Subdividing the women with PIH in relation to the presence of proteinuria (greater than or equal to 0.3 g/l), those with proteinuria, in addition to significantly higher levels of FVR and TPR, had significantly higher levels of FVT than normal pregnant women, while ANF plasma values were higher even though the difference was only near the level of significance. Hypertensive women with proteinuria also had higher values of FVT than hypertensive women without proteinuria. By means of multiple regression ANF did not show any significant correlations with hematocrit or sodium excretion. Hypertension with proteinuria seems to represent a more severe form of the disease in which, in addition to the probable influence of other factors such as the renin-angiotensin and prostaglandin systems, a greater increase in peripheral sympathetic tone than in hypertension alone appears to be present, causing a reduction in venous compliance in addition to the elevation in FVR and TPR, with increase in central blood volume and atrial stretch. This may explain the higher ANF plasma levels in these patients in comparison with normal pregnant women, even though the absence of a significant correlation of ANF with hematocrit and the fact that ANF increase was only near the level of significance may suggest a change in the relation between ANF secretion and atrial volume receptors in pregnancy either normal or complicated by hypertension. ANF does not seem to play an important role in water and sodium excretion in PIH probably because of the presence of very high plasma levels of hormones such as aldosterone, progesterone and oestriol which, together with renal prostaglandins, seem to be involved in diuresis and natriuresis in pregnancy.

Effect of increased central blood volume with water immersion on plasma catecholamines during exercise

To examine the influence of an increase in central blood volume with head-out water immersion (WI) on the sympathoadrenal response to graded dynamic exercise, nine healthy men underwent upright leg cycle exercise on land and with WI. Plasma norepinephrine and epinephrine concentrations were used as indexes of overall sympathoadrenal activity. Oxygen consumption (VO2), heart rate, systolic blood pressure, and plasma concentrations of norepinephrine, epinephrine, and lactate were determined at work loads corresponding to approximately 40, 60, 80, and 100% peak VO2. Peak VO2 did not differ on land and with WI. Plasma norepinephrine concentration was reduced (P less than 0.05) at 80 and 100% peak VO2 with WI and on land, respectively. Plasma epinephrine and lactate concentrations were similar on land and with WI at the three submaximal work stages, but both were reduced (P less than 0.05) at peak exertion with WI. Heart rate was lower (P less than 0.05) at the three highest work intensities with WI. These results suggest that the central shift in blood volume with WI reduces the sympathoadrenal response to high-intensity dynamic exercise.

Lidocaine pharmacokinetics during water immersion in normal humans.

Water immersion produces a marked diuresis, natriuresis, and kaliuresis in association with suppression of the renin-aldosterone system. These effects are mediated primarily by an increase in central blood volume. Consequently, this redistribution and the resultant marked increase in cardiac output is associated with alterations in the circulating levels of several volume regulatory hormones, including plasma renin activity and plasma aldosterone. Although the changes in these blood hormonal levels probably reflect perturbation of hormonal release, it is conceivable that the above-mentioned central hemodynamic modifications result in an altered splanchnic blood flow, thereby modulating hormonal clearances. We assessed the effects of immersion on hepatic blood flow by determining the pharmacokinetics of single doses of lidocaine administered intravenously. Seven normal male subjects were studied during a time-control period and during water immersion to the neck. The clearance of lidocaine was unaltered by immersion, suggesting that the presumed marked central hypervolemia and increased cardiac output was not associated with changes in splanchnic blood flow.

Effect of posture on the plasma levels of atrial natriuretic factor.

Atrial natriuretic factor (ANF) is a peptide with potent natriuretic, diuretic and vasorelaxant activities. Stretching of the right atria causes release of ANF into the circulation. Therefore, changes in central blood volume or acute volume expansion are likely to change the plasma levels of ANF. In this study we investigated the effects of changes in posture on the plasma levels of ANF, plasma renin activity (PRA) and plasma aldosterone (aldo). Eight male and five female volunteers ranging in age from 23 to 26 years were placed on a normal sodium intake and on the experimental day blood was obtained for ANF, PRA, and aldo after 30 minutes of lying supine, 30 minutes of 10 or 20 degrees head-down tilt, and 30 minutes of standing. Plasma ANF increased significantly after 30 minutes of head-down tilt from the supine value of 33.7 +/- 5.2 pg/ml to 47.7 +/- 7.7 pg/ml (p less than 0.02) and suppressed to 14.1 +/- 0.02) after 30 minutes of standing. PRA did not change significantly with head-down tilt, (supine 1.64 +/- 0.44 ngAI/ml/h vs. 30 minutes tilt 1.28 +/- 0.32 ngAI/ml/h (p = NS). Plasma aldosterone decreased by head-down tilt from 11.2 +/- 1.2 ng/ml to 8.4 +/- 0.8 ng/dl (p less than 0.02) and returned to the supine level after standing. In conclusion ANF levels change significantly with posture. Increase in central blood volume by head-down tilt increases ANF levels and suppresses plasma aldosterone with no effect on PRA. Standing decreases ANF significantly. These results suggest that for proper interpretation of plasma levels of ANF, posture at the time of sampling has to be standardized.