Elevated central venous pressure: A consequence of exercise training-induced hypervolemia

Resting plasma volumes, and arterial and central venous pressures (CVP) were measured in 16 men before and after exercise training to determine if training-induced hypervolemia could be explained by a change in total vascular capacitance. In addition, resting levels of plasma vasopressin (AVP), atrial natriuretic peptide (ANP), aldosterone (ALD), and norepinephrine (NE) were measured before and after training. The same measurements of vacular volume, pressures, and plasma hormones were measured in 8 subjects who did not undergo exercise and acted as controls. The exercise training program consisted of 10 weeks of controlled cycle exercise for 30 min/d, 4 d/wk at 75 to 80 percent of maximal oxygen uptake (VO2max). A training effect was verified by a 20 percent increase in VO2max, a resting bradycardia, and a 370 ml (9 percent) increase in blood volume. Mean arterial blood pressure was unaltered by exercise training, but resting CVP increased. The percent change in blood volume from before to after training was linearly related to the percent change in CVP. As a consequence of elevations in both blood volume and CVP, the volume-to-pressure ratio was essentially unchanged following exercise training. Plasma AVP, ANP, ALD, and NE were unaltered. Results indicate that elevated CVP is a consequence of training-induced hypervolemia without alteration in total effective venous capacitance. This may represent a resetting of the pressure-volume stimulus-response relation for regulation of blood volume

Effect of metal clusters on the swelling of gold-fluorocarbon-polymer composite films

We have investigated the phenomenon of swelling due to acetone diffusion in fluorocarbon polymer films doped with different gold concentrations below the percolation threshold. The presence of the gold clusters in the polymer is shown to improve the mixing between the fluorocarbon polymer and the acetone, which is not a good solvent for this kind of polymers. In order to explain the experimental results the stoichiometry and the morphology of the polymer--metal system have been studied and a modified version of the Flory--Huggins model has been developed

Comparison of Two Methods for Noninvasive Determination of Stroke Volume During Orthostatic Challenge

Background: The real time, beat-by-beat, non-invasive determination of stroke volume (SV) is an important parameter in many aerospace related physiologic protocols. In this study, we compared simultaneous estimates of SV calculated from peripheral pulse waveforms with a more conventional non-invasive technique. Methods: Using a prospective, randomized blinded protocol, ten males and nine females completed 12-mm tilt table protocols. The relative change (%(Delta)) in beat-to-beat SV was estimated non-invasively from changes in pulse waveforms measured by application of infrared finger photoplethysmography (IFP) with a Portapres(Registered TradeMark) blood pressure monitoring device and by thoracic impedance cardiography (TIC). The %(Delta) SV values were calculated from continuous SV measurements in the supine posture and over the first 10 s (T1), second 10 s (T2), and 3.5 minutes (T3) of 80deg head-up tilt (HUT). Results: The average %(Delta) SV measured by IFP at T1 (-11.7 +/- 3.7 %) was statistically less (P or = 0.322) than the average %(Delta) SV measured by TIC at T2 (-21.8 +/- 2.5 %), and T3 (-22.6 +/- 2.9 %). Correlation coefficients (r(sup 2)) between IFP and TIC were 0.117 (T1), 0.387 (T2), and 0.7 18 (T3). Conclusion: IFP provides beat-to-beat (real time) assessment of %(Delta) SV after 20 sec of transition to an orthostatic challenge that is comparable to the commonly accepted TIC. Our data support the notion that IFP technology which has flown during space missions can be used to accurately assess physiological status and countermeasure effectiveness for orth static problems that may arise in astronauts after space flight. While the peripherally measured IFP response is slightly delayed, the ease of implementing this monitor in the field is advantageous

Resting sympathetic baroreflex sensitivity in subjects with low and high tolerance to central hypovolemia induced by lower body negative pressure

Central hypovolemia elicited by orthostasis or hemorrhage triggers sympathetically-mediated baroreflex responses to maintain organ perfusion; these reflexes are less sensitive in patients with orthostatic intolerance, and during conditions of severe blood loss, may result in cardiovascular collapse (decompensatory or circulatory shock). The ability to tolerate central hypovolemia is variable and physiological factors contributing to tolerance are emerging. We tested the hypothesis that resting muscle sympathetic nerve activity (MSNA) and sympathetic baroreflex sensitivity (BRS) are attenuated in male and female subjects who have low tolerance (LT) to central hypovolemia induced by lower body negative pressure (LBNP). MSNA and diastolic arterial pressure (DAP) were recorded in 47 human subjects who subsequently underwent LBNP to tolerance (onset of presyncopal symptoms). LT subjects experienced presyncopal symptoms prior to completing LBNP of -60 mm Hg, and subjects with high tolerance (HT) experienced presyncopal symptoms after completing LBNP after -60 mmHg. Contrary to our hypothesis, resting MSNA burst incidence was not different between LT and HT subjects, and was not related to time to presyncope. BRS was assessed as the slope of the relationship between spontaneous fluctuations in DAP and MSNA during 5 min of supine rest. MSNA burst incidence/DAP correlations were greater than or equal to 0.5 in 37 subjects (LT: n= 9; HT: n=28), and BRS was not different between LT and HT (-1.8 ± 0.3 vs. -2.2 ± 0.2 bursts•(100 beats)-1•mmHg-1, p=0.29). We conclude that tolerance to central hypovolemia is not related to either resting MSNA or sympathetic BRS

Hemodynamic and ADH responses to central blood volume shifts in cardiac-denervated humans

Hemodynamic responses and antidiuretic hormone (ADH) were measured during body position changes designed to induce blood volume shifts in ten cardiac transplant recipients to assess the contribution of cardiac and vascular volume receptors in the control of ADH secretion. Each subject underwent 15 min of a control period in the seated posture, then assumed a lying posture for 30 min at 6 deg head down tilt (HDT) followed by 20 min of seated recovery. Venous blood samples and cardiac dimensions (echocardiography) were taken at 0 and 15 min before HDT, 5, 15, and 30 min of HDT, and 5, 15, and 30 min of seated recovery. Blood samples were analyzed for hematocrit, plasma osmolality, plasma renin activity (PRA), and ADH. Resting plasma volume (PV) was measured by Evans blue dye and percent changes in PV during posture changes were calculated from changes in hematocrit. Heart rate (HR) and blood pressure (BP) were recorded every 2 min. Results indicate that cardiac volume receptors are not the only mechanism for the control of ADH release during acute blood volume shifts in man

Clinical Aspects of the Control of Plasma Volume at Microgravity and During Return to One Gravity

Plasma volume is reduced by 10%-20% within 24 to 48 h of exposure to simulated or actual microgravity. The clinical importance of microgravity-induced hypovolemia is manifested by its relationship with orthostatic intolerance and reduced VO2max after return to one gravity (1G). Since there is no evidence to suggest plasma volume reduction during microgravity is associated with thirst or renal dysfunctions, a diuresis induced by an immediate blood volume shift to the central circulation appears responsible for microgravity-induced hypovolemia. Since most astronauts choose to restrict their fluid intake before a space mission, absence of increased urine output during actual spaceflight may be explained by low central venous pressure (CVP) which accompanies dehydration. Compelling evidence suggests that prolonged reduction in CVP during exposure to microgravity reflects a 'resetting' to a lower operating point which acts to limit plasma volume expansion during attempts to increase fluid intake. In groudbase and spaceflight experiments, successful restoration and maintenance of plasma volume prior to returning to an upright posture may depend upon development of treatments that can return CVP to its baseline 10 operating point. Fluid-loading and LBNP have not proved completely effective in restoring plasma volume, suggesting that they may not provide the stimulus to elevate the CVP operating point. On the other, exercise, which can chronically increase CVP, has been effective in expanding plasma volume when combined with adequate dietary intake of fluid and electrolytes. The success of designing experiments to understand the physiological mechanisms of and development of effective countermeasures for the control of plasma volume in microgravity and during return to one gravity will depend upon testing that can be conducted under standardized controlled baseline cond

Comparison of saline and fludrocortisone as fluid-loading countermeasures following exposure to simulated microgravity

Saline loading (SL) within hours of reentry is currently used as a countermeasure against postflight orthostatic hypotension in astronauts. However, its effects on blood volume expansion is not quantified and its effectiveness has proved marginal at best. The purposes of the present study were: (1) to quantify the effects of SL on plasma volume and orthostatic tolerance following exposure to simulated microgravity and (2) to compare these effects with the use of a pharacological fluid expander, fludrcortisone (F). Method: Eleven men (30-45 yr.) underwent a 15-minute stand test before and immediately after 7 days of head-down bedrest (BR). Five subjects ingested SL (8 g salt tablets with 1 liter of water) 2 hours before standing at the end of BR while the other 6 subjects received 0.2 mg oral doses of F at 0800 and 2200 hours the day before and 0800 hours the day the subjects got out of bed (i.e., 2 hours before standing). Plasma volume (PV) was measured before BR on day 7 of BR and after the final SL and F treatments just before the post-BR stand test. Blood pressure and heart rate were measured continuously during the stand tests. Results: BR decreased PV from 40.7 plus or minus 1.9 mml/kg to 35.9 plus or minus 1.1 ml/kg (minus 11.8 percent P less than 0.05). Following SL, PV remained at 36.4 plus or minus 1.5 ml/kg while F returned PV to 39.1 plus or minus 1.8 ml/kg. The post BR stand test was completed without syncopal symptoms by 5 of 6 F subjects but only 2 of 5 SL subjects. Conclusions: SL may be ineffective in restoring PV to preflight levels and may provide inadequate protection against postflight orthostatic hypotension. In contrast, F may provide a promising countermeasure since it restored PV and reduced the incidence of syncope following exposure to simulated microgravity in the present study