Cardiovascular and neuroendocrine responses to water immersion in compensated heart failure

2000 ◽  
Vol 279 (4) ◽  
pp. H1931-H1940 ◽  
Author(s):  
Anders Gabrielsen ◽  
Vibeke B. Sørensen ◽  
Bettina Pump ◽  
Søren Galatius ◽  
Regitze Videbæk ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Ejection Fraction ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Volume Expansion ◽  
Water Immersion ◽  
Central Blood Volume ◽  
Blood Volume Expansion ◽  
Neuroendocrine Responses

The hypothesis was tested that cardiovascular and neuroendocrine (norepinephrine, renin, and vasopressin) responses to central blood volume expansion are blunted in compensated heart failure (HF). Nine HF patients [New York Heart Association class II–III, ejection fraction = 0.28 ± 0.02 (SE)] and 10 age-matched controls (ejection fraction = 0.68 ± 0.03) underwent 30 min of thermoneutral (34.7 ± 0.02°C) water immersion (WI) to the xiphoid process. WI increased ( P < 0.05) central venous pressure by 3.7 ± 0.6 and 3.2 ± 0.4 mmHg and stroke volume index by 12.2 ± 2.1 and 7.2 ± 2.1 ml · beat−1 · m−2 in controls and HF patients, respectively. During WI, systemic vascular resistance decreased ( P < 0.05) similarly by 365 ± 66 and 582 ± 227 dyn · s · cm−5 in controls and HF patients, respectively. Forearm subcutaneous vascular resistance decreased by 19 ± 7% ( P < 0.05) in controls but did not change in HF patients. Heart rate decreased less during WI in HF patients, whereas release of norepinephrine, renin, and vasopressin was suppressed similarly in the two groups. We suggest that reflex control of forearm vascular beds and heart rate is blunted in compensated HF but that baroreflex-mediated systemic vasodilatation and neuroendocrine responses to central blood volume expansion are preserved.

Contribution of abdomen and legs to central blood volume expansion in humans during immersion

1997 ◽  
Vol 83 (3) ◽  
pp. 695-699 ◽  
Author(s):  
Lars Bo Johansen ◽  
Thomas Ulrik Skram Jensen ◽  
Bettina Pump ◽  
Peter Norsk
Keyword(s):  
Blood Volume ◽  
Volume Expansion ◽  
Protein Concentration ◽  
Water Immersion ◽  
Venous Pressure ◽  
Cuff Inflation ◽  
Central Blood Volume ◽  
Central Venous ◽  
Plasma Protein Concentration ◽  
Blood Volume Expansion

Johansen, Lars Bo, Thomas Ulrik Skram Jensen, Bettina Pump, and Peter Norsk. Contribution of abdomen and legs to central blood volume expansion in humans during immersion. J. Appl. Physiol. 83(3): 695–699, 1997.—The hypothesis was tested that the abdominal area constitutes an important reservoir for central blood volume expansion (CBVE) during water immersion in humans. Six men underwent 1) water immersion for 30 min (WI), 2) water immersion for 30 min with thigh cuff inflation (250 mmHg) during initial 15 min to exclude legs from contributing to CBVE (WI+Occl), and 3) a seated nonimmersed control with 15 min of thigh cuff inflation (Occl). Plasma protein concentration and hematocrit decreased from 68 ± 1 to 64 ± 1 g/l and from 46.7 ± 0.3 to 45.5 ± 0.4% ( P < 0.05), respectively, during WI but were unchanged during WI+Occl. Left atrial diameter increased from 27 ± 2 to 36 ± 1 mm ( P < 0.05) during WI and increased similarly during WI+Occl from 27 ± 2 to 35 ± 1 mm ( P < 0.05). Central venous pressure increased from −3.7 ± 1.0 to 10.4 ± 0.8 mmHg during WI ( P < 0.05) but only increased to 7.0 ± 0.8 mmHg during WI+Occl ( P < 0.05). In conclusion, the dilution of blood induced by WI to the neck is caused by fluid from the legs, whereas the CBVE is caused mainly by blood from the abdomen.

Mechanism of attenuated thirst in aging: role of central volume receptors

1997 ◽  
Vol 272 (1) ◽  
pp. R148-R157 ◽  
Author(s):  
N. S. Stachenfeld ◽  
L. DiPietro ◽  
E. R. Nadel ◽  
G. W. Mack
Keyword(s):  
Older People ◽  
Blood Volume ◽  
Volume Expansion ◽  
Water Immersion ◽  
Inhibitory Influence ◽  
Central Blood Volume ◽  
Arterial Blood ◽  
Blood Volume Expansion ◽  
Central Volume ◽  
Older Subjects

To test the hypothesis that the inhibitory action of central blood volume expansion on thirst and renal fluid regulation is attenuated with aging, we monitored the drinking and renal responses of dehydrated older (70 +/- 2 yr, n = 6) and younger (24 +/- 1 yr, n = 6) subjects during 195 min of head-out water immersion (HOI), which shifts blood centrally and increases plasma volume (PV). Subjects dehydrated by exercising for 2 h at 36 degrees C in the evening and refraining from fluids overnight before HOI in 34 degrees C water or a seated control in water perfusion suit [time control (TC)] the next morning. Ad libitum water intake was allowed after 15 min of HOI. Dehydration decreased PV by 10.6 +/- 1 and 7.3 +/- 1.8% (P < 0.05) and increased plasma osmolality by 6 +/- 2 and 7 +/- 1 mosmol/kg H2O (P < 0.05) in older and younger subjects, respectively. Thirst ratings increased in both groups, but pre-HOI thirst perception on a line rating scale was lower in older (69 +/- 8 mm) than younger (94 +/- 6 mm, P < 0.05) subjects. Fifteen minutes of HOI restored PV by 7.8 +/- 1.0 and 5.7 +/- 1.0% in older and younger subjects, respectively, but suppressed thirst rating in younger subjects only (P < 0.05). Fluid intake was reduced in HOI compared with TC in younger (6.3 +/- 0.5 vs. 14.3 +/- 2.2 ml/kg, P < 0.05) but not in older (6.7 +/- 2.1 vs. 8.4 +/- 3.3 ml/kg) subjects. During HOI, older subjects had smaller suppression of plasma renin activity and aldosterone concentration but a greater increase in the plasma atrial natriuretic peptide concentration (P[ANP], P < 0.05). HOI increased fractional sodium excretion in both groups, but mean arterial pressure increased only in the older subjects (P < 0.05). We conclude that the inhibitory influence of central volume expansion on thirst and drinking behavior is diminished with aging. Furthermore, in contrast to younger people, HOI natriuresis is associated with exaggerated increases in P[ANP] and arterial blood pressure in older people, suggesting arterial baroreceptors may be involved in the fluid regulatory response to central blood volume expansion in older people.

Effects of central venous blood volume shifts on arterial baroreflex control of heart rate

1981 ◽  
Vol 241 (4) ◽  
pp. H571-H575 ◽  
Author(s):  
G. E. Billman ◽  
D. T. Dickey ◽  
K. K. Teoh ◽  
H. L. Stone
Keyword(s):  
Heart Rate ◽  
Blood Volume ◽  
Volume Expansion ◽  
Body Position ◽  
Venous Blood ◽  
Receptor Blockade ◽  
Baroreflex Control ◽  
Beta Receptor ◽  
Blood Volume Expansion ◽  
Beta Receptor Blockade

The purpose of this study was to investigate the effects of anesthesia, body position, and blood volume expansion on baroreflex control of heart rate. Five male rhesus monkeys (7.0-10.5 kg) were given bolus injection of 4.0 micrograms/kg phenylephrine during each of the following situations: awake sitting, anesthetized (AN) (10 mg/kg ketamine-HCl) sitting, AN recumbent, AN 90 degrees head down tilt, and AN 50% blood volume expansion with normal saline. beta-Receptor blockade was also performed on each treatment after anesthesia. Four additional animals were similarly treated after 20% blood volume expansion. R-R interval was plotted against systolic aortic pressure, and the slope was determined by linear regression. Baroreflex slope was significantly (P less than 0.05) reduced by 90 degrees head down tilt and 50% volume expansion both before and after beta-receptor blockade. A similar trend was seen after 20% volume expansion. These data are consistent with the thesis that baroreflex control of heart rate is reduced by central blood volume shifts.

Baroreflex regulation of hindquarter vascular resistance during acute blood volume expansion

1984 ◽  
Vol 246 (1) ◽  
pp. H74-H79 ◽  
Author(s):  
G. B. Guo ◽  
D. R. Richardson
Keyword(s):  
Blood Volume ◽  
Vascular Resistance ◽  
Volume Expansion ◽  
Time Course ◽  
Venous Pressure ◽  
Systemic Arterial Pressure ◽  
Baroreflex Control ◽  
Blood Volume Expansion ◽  
Cardiopulmonary Receptors ◽  
Cardiopulmonary Baroreceptors

The baroreflex control of hindquarter vascular resistance in response to a 30% blood volume expansion (BVE) was examined in constant-flow perfused hindlimbs of chloralose-urethan-anesthetized rats. Volume expansion initially increased both systemic arterial pressure (SAP) and central venous pressure (CVP) while decreasing hindquarter vascular resistance. After these initial changes, there was a parallel return of hindquarter-vascular resistance and CVP to pre-expansion levels, suggesting that cardiopulmonary afferents play a major role in the vascular resistance adjustments to volume expansion. This notion was supported in a separate set of experiments in which CVP was elevated selectively while SAP was held constant. This manipulation elicited a decrease in hindquarter vascular resistance, which was significantly attenuated following vagal cardiopulmonary denervation. The return of hindquarter vascular resistance following BVE also occurred in the presence of elevated SAP in rats with vagotomy and aortic nerve denervation, i.e., only the carotid sinus baroreflexes intact, but the time course was much faster compared with preparations with cardiopulmonary receptors intact. No response of hindquarter vascular resistance to BVE was observed in rats with both sinoaortic and cardiopulmonary baroreceptors denervated. These findings suggest that the return of hindquarter vascular resistance following BVE involves a gradual increase in sympathetic outflow to the hindquarters resulting from both a decrease in cardiopulmonary afferent activity and a rapid adaptation of arterial baroreflexes.

Hypotension produced by vagal block in primates

1988 ◽  
Vol 254 (6) ◽  
pp. R857-R862
Author(s):  
K. G. Cornish ◽  
M. Barazanji ◽  
A. Ryberg ◽  
J. P. Gilmore
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Left Atrial ◽  
Volume Expansion ◽  
Water Immersion ◽  
Abdominal Cavity ◽  
Sympathetic Tone ◽  
Control Group ◽  
Blood Volume Expansion ◽  
Cardiopulmonary Receptors

In many species, the vagus has been reported to contain afferents that inhibit sympathetic tone. Vagal block (VB) increases blood pressure in both the intact and sinoaortic-denervated (SAD) dog. In the present study, VB was produced in intact and SAD monkeys by infiltrating the vagi with a local anesthetic. This was done in conjunction with blood volume expansion or head-out water immersion. The cardiovascular parameters monitored were heart rate (HR), blood pressure (BP), and left atrial pressure (LAP). VB decreased BP (-13 +/- 2.8 mmHg) in the control group and the SAD animals (-47 +/- 6.7 mmHg) without changing HR. Volume expansion decreased BP in the SAD animals (-6 +/- 3.4) but not in the intact monkeys (1.8 +/- 2.27), whereas HR did not change. Volume expansion after VB increased BP in both the SAD and the intact animals while producing a decrease in HR. Volume expansion caused LAP to increase in all groups (SAD 13.9 +/- 6.3; control VB 11.6 +/- 1.8, control 9.3 +/- 0.89, SAD VB 7.66 +/- 3.46). Immersion in the VB SAD animals increased BP to a greater extent than volume expansion. VB in the monkey must be removing input from peripheral receptors, which maintain sympathetic tone. Because immersion with VB increases BP more than volume expansion with VB, it is concluded that VB causes predominantly venous pooling. Because cardiopulmonary receptors generally inhibit sympathetic tone, it is concluded that those receptors responsible for the observed hypotension are located in the venous system, probably in the chest or the abdominal cavity.

Effect of central hypervolemia on cardiac performance during exercise

1984 ◽  
Vol 57 (6) ◽  
pp. 1662-1667 ◽  
Author(s):  
L. M. Sheldahl ◽  
L. S. Wann ◽  
P. S. Clifford ◽  
F. E. Tristani ◽  
L. G. Wolf ◽  
...  
Keyword(s):  
Heart Rate ◽  
Blood Volume ◽  
Water Immersion ◽  
Left Ventricular ◽  
Cardiac Performance ◽  
Central Blood Volume ◽  
Supine Posture ◽  
Left Ventricular Dimensions ◽  
Submaximal Work ◽  
And Performance

To investigate the effect of different levels of central blood volume on cardiac performance during exercise, M-mode echocardiography was utilized to determine left ventricular size and performance during cycling exercise in the upright posture (UP), supine posture (SP), and head-out water immersion (WI). At submaximal work loads requiring a mean O2 consumption (Vo2) of 1.2 1/min and 1.5 1/min, mean left ventricular end-diastolic and end-systolic dimensions were significantly greater (P less than 0.05) with WI than UP. In the SP during exercise, left ventricular dimensions were intermediate between UP and WI. Heart rate did not differ significantly among the three conditions at rest and at submaximal exercise up to a mean Vo2 of 1.8 1/min. However, at a mean Vo2 of 2.4 1/min, heart rate in the UP was significantly greater than WI (P less than 0.01) and the SP (P less than 0.05). Maximal Vo2 did not differ statistically in the three conditions. These data indicate that a change in central blood volume results in alterations in left ventricular end-diastolic and end-systolic dimensions during moderate levels of exercise and a change in heart rate at heavy levels of exercise.

Effects of Acute Blood Volume Expansion on Vascular Resistance and Reactivity in Anaesthetized Dogs

1983 ◽  
Vol 65 (1) ◽  
pp. 9-17 ◽  
Author(s):  
Bhagavan S. Jandhyala ◽  
Gary J. Hom
Keyword(s):  
Angiotensin Ii ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Volume Expansion ◽  
Hind Limb ◽  
Donor Blood ◽  
Response Curves ◽  
Circulating Blood Volume ◽  
Functional Changes ◽  
Blood Volume Expansion

1. The effects of acute volume expansion on vascular resistance and reactivity to noradrenaline and angiotensin II are reported in this study. The estimated circulating blood volume of pentobartibal-anaesthetized dogs was expanded by about 35% with equilibrated donor blood. The animals were bilaterally nephrectomized to sustain expanded volume. 2. Functional changes in vascular smooth muscle were determined in the flow controlled, vascularly isolated, denervated, perfused hind limb preparation in the same animal. 3. Systemic volume expansion per se had no immediate influence on vascular resistance. However, resistance in the hind limb, as determined by the shift of the pressure-flow curves, progressively increased 60 and 120 min after volume expansion. The changes noted after 120 min were significantly greater than those observed after 60 min. 4. The changes in vascular resistance were accompanied by potentiation of the vascular responses to noradrenaline but not to angiotensin II. Significant shifts which occurred in the noradrenaline dose-response curves were similar to those of the resistance curves. 5. in closely simulated control experiments in dogs whose kidneys were intact or had been removed, and whose blood had or had not been equilibrated with donor blood, the above-mentioned vascular changes were not observed in the absence of volume expansion. 6. It is suggested that the functional changes observed in the hind limb vasculature after volume expansion are related to the presence of a circulating substance. From the data obtained from the experimental model used in this study, it can be concluded that such a substance is not released from the kidney.

Cardiac performance: independent effects of inotropy and preload at high heart rate

1979 ◽  
Vol 236 (4) ◽  
pp. H568-H576
Author(s):  
A. Ilebekk ◽  
M. M. Miller ◽  
F. Kiil
Keyword(s):  
Heart Rate ◽  
Blood Volume ◽  
Volume Expansion ◽  
Left Ventricular ◽  
Right Atrial ◽  
High Heart Rate ◽  
Atrial Pacing ◽  
Adrenergic Stimulation ◽  
End Diastolic Volume ◽  
Blood Volume Expansion

Linear relationships between stroke volume (SV) and heart rate (HR) were observed during right atrial pacing in open-chest dogs at control inotropy, during intravenous isoproterenol infusion and during blood volume expansion by saline infusion at HR exceeding 150 beats/min. The slope of these relationships remained constant during variations in inotropy, but rose during blood volume expansion. Myocardial chord lengths in the anterior left ventricular wall were continuously recored by ultrasonic technique to estimate left ventricular volume. When heart rate was increased, end-diastolic volume decreased more rapidly after than before blood volume expansion, explaining the increased slope of the SV/HR relationship. The end-diastolic volume and the SV/HR relationship were not influenced by changes in inotropy. After blood volume expansion by 57 +/- 13%, control end-diastolic volume was reestablished by increasing heart rate 84 +/- 20 beats/min. At identical end-diastolic volume, SV was equal at different HR. Thus, the effects on SV of changes in preload and inotropy are separable during right atrial pacing, and SV is independent of HR at constant preload and adrenergic stimulation.

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

1990 ◽  
Vol 69 (2) ◽  
pp. 651-656 ◽  
Author(s):  
T. P. Connelly ◽  
L. M. Sheldahl ◽  
F. E. Tristani ◽  
S. G. Levandoski ◽  
R. K. Kalkhoff ◽  
...  
Keyword(s):  
Heart Rate ◽  
Blood Volume ◽  
Water Immersion ◽  
Plasma Concentrations ◽  
Plasma Catecholamines ◽  
Dynamic Exercise ◽  
Plasma Norepinephrine ◽  
Central Blood Volume ◽  
Peak Vo2 ◽  
Sympathoadrenal Activity

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.

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