Plasma volume shifts during progressive arm and leg exercise

1983 ◽  
Vol 54 (2) ◽  
pp. 491-495 ◽  
Author(s):  
D. S. Miles ◽  
M. N. Sawka ◽  
R. M. Glaser ◽  
J. S. Petrofsky
Keyword(s):  
Mean Arterial Pressure ◽  
Oxygen Uptake ◽  
Arterial Pressure ◽  
Plasma Volume ◽  
Relative Intensity ◽  
Lower Body ◽  
Leg Exercise ◽  
Intensity Of Exercise ◽  
Plasma Volume Shifts ◽  
Male Subjects

Upper and lower body exercise was performed to assess the influence muscle mass has on plasma volume (PV) shifts. Nine male subjects (mean = 28 yr) completed a progressive intensity, discontinuous test with an arm crank (AC) and cycle (CY) ergometer. Power output (PO) levels for the AC were 25, 74, 98, and 133 W. PO levels for the CY were 49, 98, 147, and 263 W. At a given submaximal oxygen uptake (VO2), PV efflux was significantly greater for AC compared with CY exercise. When PV efflux was related to the relative intensity of the exercise (ergometer specific % peak VO2), responses were nearly identical. Maximal PV efflux was 18% for both AC and CY exercise. Mean arterial pressure (MAP) was significantly greater for AC compared with CY exercise for a given VO2. MAP plotted against the relative intensity of exercise, however, was similar for both AC and CY exercise. These results suggest that the amount of plasma efflux during exercise is related to the MAP, which is directly related to the relative intensity of the exercise.

Effect of Noise on Blood Pressure and ‘Stress’ Hormones

1982 ◽  
Vol 62 (2) ◽  
pp. 137-141 ◽  
Author(s):  
L. Andrén ◽  
G. Lindstedt ◽  
M. Björkman ◽  
K. O. Borg ◽  
L. Hansson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Growth Hormone ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Systolic Blood Pressure ◽  
Stress Hormones ◽  
Significant Change ◽  
Male Subjects ◽  
Venous Plasma

1. Noise stimulation (95 dBA) for 20 min caused a significant increase in diastolic (12%, P < 0.001) and mean arterial pressure (7%, P < 0.001) in 15 healthy normotensive male subjects. 2. There was no significant change in systolic blood pressure or heart rate during exposure to noise. 3. Adrenaline, noradrenaline, prolactin, cortisol and growth hormone concentrations in venous plasma were not affected during noise stimulation.

Cardiovascular responses to lower body negative pressure in trained and untrained older men

1992 ◽  
Vol 73 (6) ◽  
pp. 2693-2700 ◽  
Author(s):  
S. Fortney ◽  
C. Tankersley ◽  
J. T. Lightfoot ◽  
D. Drinkwater ◽  
J. Clulow ◽  
...  
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Older Men ◽  
Volume Index ◽  
Lower Body ◽  
Vo2 Max ◽  
Cardiac Volumes

To determine whether aerobic conditioning alters the orthostatic responses of older subjects, cardiovascular performance was monitored during graded lower body negative pressure in nine highly trained male senior athletes (A) aged 59–73 yr [maximum O2 uptake (VO2 max) = 52.4 +/- 1.7 ml.kg-1 x min-1] and nine age-matched control subjects (C) (VO2 max = 31.0 +/- 2.9 ml.kg-1 x min-1). Cardiac volumes were determined from gated blood pool scintigrams by use of 99mTc-labeled erythrocytes. During lower body negative pressure (0 to -50 mmHg), left ventricular end-diastolic and end-systolic volume indexes and stroke volume index decreased in both groups while heart rate increased. The decreases in cardiac volumes and mean arterial pressure and the increase in heart rate between 0 and -50 mmHg were significantly less in A than in C. For example, end-diastolic volume index decreased by 32 +/- 4 ml in C vs. 14 +/- 2 ml in A (P < 0.01), mean arterial pressure declined 7 +/- 5 mmHg in C and increased by 5 +/- 3 mmHg in A (P < 0.05), and heart rate increased 13 +/- 3 beats/min in C and 7 +/- 1 beats/min in A (P < 0.05). These data suggest that increased VO2 max among older men is associated with improved orthostatic responses.

Effects of V1- and V2-vasopressin (AVP) antagonists on the pressor, AVP and atrial natriuretic peptide responses to a hypertonic saline infusion in conscious anephric rats

1995 ◽  
Vol 133 (1) ◽  
pp. 127-132 ◽  
Author(s):  
Kozo Ota ◽  
Tokihisa Kimura ◽  
Minoru Inoue ◽  
Takeharu Funyu ◽  
Masaru Shoji ◽  
...  
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Receptor Antagonist ◽  
Hypertonic Saline ◽  
Natriuretic Peptide ◽  
Plasma Volume ◽  
Control Group ◽  
Antagonist Group

Ota K, Kimura T, Inoue M, Funyu T, Shoji M, Sato K, Ohta M, Yamamoto T, Abe K, Effects of V1- and V2-vasopressin (AVP) antagonists on the pressor, AVP and atrial natriuretic peptide responses to a hypertonic saline infusion in conscious anephric rats. Eur J Endocrinol 1995;133:127–32. ISSN 0804–4643 To examine the role of vasopressin (AVP) receptors in the regulation of the hemodynamics and release of atrial natriuretic peptide (ANP), and the participation of renal nerve inputs in the osmotic AVP release, hypertonic saline (HS) was infused into conscious, bilaterally nephrectomized rats with nonpeptide, selective antagonists for the V1-receptor or V2-receptor of AVP. In the control group, HS alone increased mean arterial pressure, plasma ANP and AVP, plasma volume and plasma osmolality, and decreased the heart rate. In the V1-receptor antagonist group, an increase in the mean arterial pressure and a decrease in heart rate were completely abolished and an increase in plasma ANP was attenuated. In the V2-receptor antagonist group, increases in mean arterial pressure and plasma ANP and a decrease in heart rate were attenuated. However, the ratio of the changes in heart rate to the changes in mean arterial pressure in the V2-receptor antagonist group is significantly higher than that in the control group. In both experimental groups, increases in plasma AVP, plasma volume and plasma osmolality were not different from those in the control group. These results suggest that a HS-induced increase in mean arterial pressure is mediated by the pressor effect of AVP, mainly through V1-receptors, and that the depressor effect of AVP through V2-receptors may not influence tonically HS-induced hypertension. Moreover, HS-induced increase in plasma ANP is mediated mainly by increases in plasma volume and blood pressure, but may not be affected by a direct action of AVP to the heart. Renal afferent nerve inputs may not have effects on the regulation of osmotic AVP release. Kozo Ota, Second Department of Internal Medicine, Tohoku University School of Medicine, 1-1 Seiryo-cho, Aoba-ku, Sendai 980-77, Japan

Baroreceptor-mediated suppression of osmotically stimulated vasopressin in normal humans

1988 ◽  
Vol 65 (3) ◽  
pp. 1226-1230 ◽  
Author(s):  
S. R. Goldsmith
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Central Venous Pressure ◽  
Venous Pressure ◽  
Positive Pressure ◽  
Lower Body ◽  
Central Venous ◽  
Lower Body Positive Pressure ◽  
Body Positive

Increases in central venous pressure and arterial pressure have been reported to have variable effects on normal arginine vasopressin (AVP) levels in healthy humans. To test the hypothesis that baroreceptor suppression of AVP secretion might be more likely if AVP were subjected to a prior osmotic stimulus, we investigated the response of plasma AVP to increased central venous pressure and mean arterial pressure after hypertonic saline in six normal volunteers. Plasma AVP, serum osmolality, heart rate, central venous pressure, mean arterial pressure, and pulse pressure were assessed before and after a 0.06 ml.kg-1.min-1-infusion of 5% saline give over 90 min and then after 10 min of 30 degrees head-down tilt and 10 min of head-down tilt plus lower-body positive pressure. Hypertonic saline increased plasma AVP. After head-down tilt, which did not change heart rate, pulse pressure, or mean arterial pressure but did increase central venous pressure, plasma AVP fell. Heart rate, pulse pressure, and central venous pressure were unchanged from head-down tilt values during lower-body positive pressure, whereas mean arterial pressure increased. Plasma AVP during lower-body positive pressure was not different from that during tilt. Osmolality increased during the saline infusion but was stable throughout the remainder of the study. These data therefore suggest that an osmotically stimulated plasma AVP level can be suppressed by baroreflex activation. Either the low-pressure cardiopulmonary receptors (subjected to a rise in central venous pressure during head-down tilt) or the sinoaortic baroreceptors (subjected to hydrostatic effects during head-down tilt) could have been responsible for the suppression of AVP.(ABSTRACT TRUNCATED AT 250 WORDS)

Plasma Volume Decrease and Elevated Evans Blue Disappearance Rate in Essential Hypertension

1973 ◽  
Vol 45 (2) ◽  
pp. 173-181 ◽  
Author(s):  
Milos Ulrych
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Essential Hypertension ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Volume ◽  
Evans Blue ◽  
Disappearance Rate ◽  
The Mean ◽  
Volume Decrease

1. The disappearance rate of intravenously injected Evans Blue, plasma volume, cardiac output, and blood pressure were measured in seven normotensive and eighteen hypertensive subjects. 2. Plasma volume was found to be negatively correlated with the mean arterial pressure, Evans Blue disappearance rate and packed cell volume. 3. Faster disappearance rate of Evans Blue in hypertensive subjects may be due to an abnormality of mixing of the label or of the capillaries.

Muscle sympathetic nerve responses to static leg exercise

1992 ◽  
Vol 73 (4) ◽  
pp. 1523-1529 ◽  
Author(s):  
C. A. Ray ◽  
R. F. Rea ◽  
M. P. Clary ◽  
A. L. Mark
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Circulatory Arrest ◽  
Knee Extension ◽  
Voluntary Contraction ◽  
Leg Exercise

Previous studies of muscle sympathetic nerve activity (MSNA) during static exercise have employed predominantly the arms. These studies have revealed striking increases in arm and leg MSNA during static handgrip (SHG) and postexercise circulatory arrest (PECA). The purpose of this study was to examine MSNA during static leg exercise (SLE) at intensities and duration commonly used during SHG followed by PECA. During 2 min of SLE (static knee extension) at 10% of maximal voluntary contraction (MVC; n = 18) in the sitting position, mean arterial pressure and heart rate increased significantly. Surprisingly, MSNA in the contralateral leg did not increase above control levels during SLE but rather decreased (23 +/- 5%; P < 0.05) during the 1st min of SLE at 10% MVC. We compared MSNA responses to SHG and SLE (n = 8) at 30% MVC. SHG and SLE elicited comparable increases (P < 0.05) in arterial pressure and heart rate, but SHG elicited significant increases in MSNA, whereas SLE did not. During PECA after SHG and SLE, mean arterial pressure remained significantly above control. However, MSNA was unchanged during PECA after SLE but was significantly greater than control during PECA after SHG. Because previous studies have indicated differences in MSNA responses to the arm and leg, we measured arm and leg MSNA simultaneously in six subjects during SLE at 20% MVC and PECA. During SLE and PECA, MSNA in the contralateral arm and leg did not differ significantly from each other.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Plasma hyperosmolality improves tolerance to combined heat stress and central hypovolemia in humans

2017 ◽  
Vol 312 (3) ◽  
pp. R273-R280 ◽  
Author(s):  
Daniel Gagnon ◽  
Steven A. Romero ◽  
Hai Ngo ◽  
Paula Y. S. Poh ◽  
Craig G. Crandall
Keyword(s):  
Heart Rate ◽  
Heat Stress ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve Activity ◽  
Lower Body Negative Pressure ◽  
Muscle Sympathetic Nerve Activity ◽  
Plasma Osmolality ◽  
Lower Body ◽  
Nerve Activity

Heat stress profoundly impairs tolerance to central hypovolemia in humans via a number of mechanisms including heat-induced hypovolemia. However, heat stress also elevates plasma osmolality; the effects of which on tolerance to central hypovolemia remain unknown. This study examined the effect of plasma hyperosmolality on tolerance to central hypovolemia in heat-stressed humans. With the use of a counterbalanced and crossover design, 12 subjects (1 female) received intravenous infusion of either 0.9% iso-osmotic (ISO) or 3.0% hyperosmotic (HYPER) saline. Subjects were subsequently heated until core temperature increased ~1.4°C, after which all subjects underwent progressive lower-body negative pressure (LBNP) to presyncope. Plasma hyperosmolality improved LBNP tolerance (ISO: 288 ± 193 vs. HYPER: 382 ± 145 mmHg × min, P = 0.04). However, no differences in mean arterial pressure ( P = 0.10), heart rate ( P = 0.09), or muscle sympathetic nerve activity ( P = 0.60, n = 6) were observed between conditions. When individual data were assessed, LBNP tolerance improved ≥25% in eight subjects but remained unchanged in the remaining four subjects. In subjects who exhibited improved LBNP tolerance, plasma hyperosmolality resulted in elevated mean arterial pressure (ISO: 62 ± 10 vs. HYPER: 72 ± 9 mmHg, P < 0.01) and a greater increase in heart rate (ISO: +12 ± 24 vs. HYPER: +23 ± 17 beats/min, P = 0.05) before presyncope. No differences in these variables were observed between conditions in subjects that did not improve LBNP tolerance (all P ≥ 0.55). These results suggest that plasma hyperosmolality improves tolerance to central hypovolemia during heat stress in most, but not all, individuals.

scholarly journals High versus low ultrafiltration rates during experimental peritoneal dialysis in rats: Acute effects on plasma volume and systemic haemodynamics

2022 ◽  
pp. 089686082110692
Author(s):  
Jakob Helman ◽  
Carl M Öberg
Keyword(s):  
Peritoneal Dialysis ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Central Venous Pressure ◽  
Plasma Volume ◽  
Venous Pressure ◽  
Extracellular Fluid ◽  
Extracellular Fluid Volume ◽  
Central Venous ◽  
Plasma Compartment

Introduction: Intradialytic hypotension is a common complication of haemodialysis, but uncommon in peritoneal dialysis (PD). This may be due to lower ultrafiltration rates in PD compared to haemodialysis, allowing for sufficient refilling of the blood plasma compartment from the interstitial volume, but the underlying mechanisms are unknown. Here we assessed plasma volume and hemodynamic alterations during experimental PD with high versus low ultrafiltration rates. Methods: Experiments were conducted in two groups of healthy Sprague-Dawley rats: one group with a high ultrafiltration rate ( N = 7) induced by 8.5% glucose and a low UF group ( N = 6; 1.5% glucose), with an initial assessment of the extracellular fluid volume, followed by 30 min PD with plasma volume measurements at baseline, 5, 10, 15 and 30 min. Mean arterial pressure, central venous pressure and heart rate were continuously monitored during the experiment. Results: No significant changes over time in plasma volume, mean arterial pressure or central venous pressure were detected during the course of the experiments, despite an ultrafiltration (UF) rate of 56 mL/h/kg in the high UF group. In the high UF group, a decrease in extracellular fluid volume of −7 mL (−10.7% (95% confidence interval: −13.8% to −7.6%)) was observed, in line with the average UF volume of 8.0 mL (standard deviation: 0.5 mL). Conclusion: Despite high UF rates, we found that plasma volumes were remarkably preserved in the present experiments, indicating effective refilling of the plasma compartment from interstitial tissues. Further studies should clarify which mechanisms preserve the plasma volume during high UF rates in PD.

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