scholarly journals Aging Decreases Hand Volume Expansion with Water Immersion

2018 ◽  
Vol 9 ◽  
Author(s):  
Jamila H. Siamwala ◽  
Davina G. Moossazadeh ◽  
Timothy R. Macaulay ◽  
Rachel L. Becker ◽  
Rekha H. Hargens ◽  
...  
Keyword(s):  
Volume Expansion ◽  
Water Immersion ◽  
Hand Volume

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.

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

1983 ◽  
Vol 244 (4) ◽  
pp. R481-R486 ◽  
Author(s):  
G. G. Krishna ◽  
G. M. Danovitch
Keyword(s):  
Sodium Excretion ◽  
Volume Expansion ◽  
Filtration Rate ◽  
Water Immersion ◽  
Peak Level ◽  
Diurnal Variations ◽  
Regulatory Mechanisms ◽  
Electrolyte Excretion ◽  
Renal Response ◽  
Central Volume

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.

Impaired sodium excretion in response to volume expansion induced by water immersion in insulin-dependent diabetes mellitus

1986 ◽  
Vol 71 (4) ◽  
pp. 403-409 ◽  
Author(s):  
J. P. O'Hare ◽  
J. M. Roland ◽  
G. Walters ◽  
R. J. M. Corrall
Keyword(s):  
Normal Control ◽  
Volume Expansion ◽  
Water Immersion ◽  
Normal Subjects ◽  
Diabetic Group ◽  
Dependent Diabetes Mellitus ◽  
Renal Response ◽  
Control Subjects ◽  
Fractional Excretion Of Sodium ◽  
Insulin Dependent

1. The renal response to volume expansion produced by water immersion to the neck at 35°C was examined in eight young normotensive uncomplicated insulin-dependent diabetic subjects and in eight matched normal control subjects. 2. Both the diabetic and normal subjects manifested a renal response of natriuresis and kaliuresis on immersion, but the natriuretic response was reduced in the diabetic group. Thus the induced excretion of sodium over the 4 h of immersion was 40 ± 5 mmol (mean ± sem) in the normal group compared with 22 ± 4 mmol in the diabetic group (P < 0.02). 3. In the normal subjects creatinine clearance did not change during immersion compared with pre-immersion control values while in the diabetic group it rose from pre-immersion control values of 112 ± 11 ml/min to a mean value of 127 ± 11 ml/min during immersion (P < 0.01). 4. The diabetic subjects thus excreted less sodium despite an increased filtered load during water immersion. Fractional excretion of sodium was significantly reduced in the diabetic subjects compared with the normal control subjects (P < 0.05). 5. The suppression of plasma renin and aldosterone was similar in normal and diabetic groups. 6. Tubular sodium retention could be an early functional change in the diabetic kidney, and be implicated in the development of diabetic nephropathy.

Dissociation of Renin-Aldosterone and Renal Prostaglandin E during Volume Expansion Induced by Immersion in Normal Man

1980 ◽  
Vol 59 (1) ◽  
pp. 55-62 ◽  
Author(s):  
M. Epstein ◽  
M. D. Lifschitz ◽  
R. Re ◽  
E. Haber
Keyword(s):  
Plasma Renin Activity ◽  
Volume Expansion ◽  
Water Immersion ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Prostaglandin E ◽  
Plasma Aldosterone Concentration ◽  
Normal Man

1. The relationship of the renin-angiotensin-aldosterone axis with renal prostaglandin E is complex. Although studies have suggested that these two hormonal systems respond to experimental manipulations in a parallel manner, their interdependence has not been assessed fully during volume expansion. Since studies have demonstrated that in normal man the central hypervolaemia induced by water immersion to the neck produces a prompt and profound suppression of plasma renin activity and plasma aldosterone concentration without concomitant alteration of plasma composition, immersion afforded a unique opportunity to assess simultaneously the effects of central hypervolaemia on plasma renin activity, plasma aldosterone concentration and prostaglandin E excretion. 2. Seven normal subjects were studied twice while in balance on a diet containing 10 mmol of sodium/day, 100 mmol of potassium/day: with indomethacin administration (50 mg given every 6 h for five doses) and without indomethacin. Urinary prostaglandin E excretion was measured hourly and plasma renin activity and plasma aldosterone concentration at 30 min intervals. 3. Immersion was associated with a marked suppression of plasma renin activity (59 ± 7%) and plasma aldosterone concentration (55 ± 3%) with a return to pre-study values during the recovery hour. Concomitantly, urinary prostaglandin E excretion increased from 4.7 to a peak of 10.9 ng/min. Although administration of indomethacin lowered the basal rate of urinary prostaglandin E excretion and plasma renin activity, it did not prevent the subsequent augmentation of urinary prostaglandin E or the suppression of plasma renin activity and plasma aldosterone during the subsequent 4 h of immersion. 4. These results demonstrate a dissociation of renin-aldosterone and prostaglandin E during hypervolaemia and suggest that whereas prostaglandin E may constitute one of the major determinants of renin release clinically and experimentally, these two hormonal systems can be dissociated from each other in response to central volume expansion in man.

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.

Neuroendocrine and renal effects of intravascular volume expansion in compensated heart failure

2001 ◽  
Vol 281 (2) ◽  
pp. R459-R467 ◽  
Author(s):  
Anders Gabrielsen ◽  
Peter Bie ◽  
Niels Henrik Holstein-Rathlou ◽  
Niels Juel Christensen ◽  
Jørgen Warberg ◽  
...  
Keyword(s):  
Heart Failure ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Water Immersion ◽  
Free Water ◽  
Ang Ii ◽  
Free Water Clearance ◽  
Fractional Sodium Excretion ◽  
Control Subjects ◽  
Water Clearance

To examine if the neuroendocrine link between volume sensing and renal function is preserved in compensated chronic heart failure [HF, ejection fraction 0.29 ± 0.03 (mean ± SE)] we tested the hypothesis that intravascular and central blood volume expansion by 3 h of water immersion (WI) elicits a natriuresis. In HF, WI suppressed ANG II and aldosterone (Aldo) concentrations, increased the release of atrial natriuretic peptide (ANP), and elicited a natriuresis ( P < 0.05 for all) compared with seated control. Compared with control subjects ( n = 9), ANG II, Aldo, and ANP concentrations were increased ( P < 0.05) in HF, whereas absolute and fractional sodium excretion rates were attenuated [47 ± 16 vs. 88 ± 15 μmol/min and 0.42 ± 0.18 vs. 0.68 ± 0.12% (mean ± SE), respectively, both P < 0.05]. When ANG II and Aldo concentrations were further suppressed ( P < 0.05) during WI in HF (by sustained angiotensin-converting enzyme inhibitor therapy, n = 9) absolute and fractional sodium excretion increased ( P < 0.05) to the level of control subjects (108 ± 34 μmol/min and 0.70 ± 0.23%, respectively). Renal free water clearance increased during WI in control subjects but not in HF, albeit plasma vasopressin concentrations were similar in the two groups. In conclusion, the neuroendocrine link between volume sensing and renal sodium excretion is preserved in compensated HF. The natriuresis of WI is, however, modulated by the prevailing ANG II and Aldo concentrations. In contrast, renal free water clearance is attenuated in response to volume expansion in compensated HF despite normalized plasma AVP concentrations.

Comparison of water immersion and saline infusion as a means of inducing volume expansion in man

1975 ◽  
Vol 39 (1) ◽  
pp. 66-70 ◽  
Author(s):  
M. Epstein ◽  
D. S. Pins ◽  
R. Arrington ◽  
A. G. Denunzio ◽  
R. Engstrom
Keyword(s):  
Volume Expansion ◽  
Water Immersion ◽  
Extracellular Fluid ◽  
Saline Infusion ◽  
Total Blood Volume ◽  
Concomitant Increase ◽  
Total Blood ◽  
Recumbent Posture ◽  
Saline Administration ◽  
Central Hypervolemia

Although previous studies have demonstrated that water immersion to the neck (NI) results in both central hypervolemia and a significant natriuresis, it is unclear whether the magnitude of the “volume stimulus” of NI is comparable to that induced by the extracellular fluid volume expansion (ECVE) induced by acute saline administration. The present study was undertaken therefore to compare the natriuresis induced by these two different stimuli. All subjects were studied on four occasions while in balance on a diet containing 150 meq of sodium and 80 meq of potassium daily: seated control; seated immersion; and saline administration in both the seated and recumbent posture. The increment in UNaV during NI was indistinguishable from that of seated saline. Similarly, the kaliuretic response during NI was similar to that induced by seated saline infusion. In contrast, supine saline infusion resulted in a greater increment in UNaV than either NI or seated saline. The present data indicate that the “volume stimulus” of immersion is identical with that of standard saline-induced ECVE in normal seated subjects. Furthermore, the ability of NI to induce a natriuresis without a concomitant increase in total blood volume and with a decrease in body weight, rather than the increase which attends saline infusion, suggests that NI may be a preferred investigative tool for assessing the effects of ECVE in man.

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.

Thiazolidinediones and the renal and hormonal response to water immersion-induced volume expansion in type 2 diabetes mellitus

2008 ◽  
Vol 294 (4) ◽  
pp. E733-E739 ◽  
Author(s):  
Niru Goenka ◽  
Christina Kotonya ◽  
Michael D. Penney ◽  
Harpal S. Randeva ◽  
J. Paul O'Hare
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Volume Expansion ◽  
Water Immersion ◽  
Guanosine Monophosphate ◽  
Significant Difference ◽  
Response To Water ◽  
Type 2 Diabetic

Thiazolidinediones cause sodium retention and edema by a direct effect on the kidneys. The aim of this study was to use the technique of head-out water immersion to investigate the effects of rosiglitazone on sodium and volume homeostasis in subjects with type 2 diabetes mellitus. The volume expansion response to water immersion was compared with the response on a non-immersion control day in 12 nondiabetic male subjects and 8 diet-controlled male type 2 diabetic subjects with hourly blood and urine sampling over a 4-h period. This was repeated after both groups had taken 4 mg of rosiglitazone daily for 7 days. Immersion produced a natriuresis in both groups ( P < 0.001). An impairment of this natriuresis was seen in the diabetic subjects ( P = 0.006). However, when rosiglitazone was taken, there was no significant difference in immersion-induced natriuresis compared with nondiabetic controls ( P = 0.2). There was an immersion-induced rise in atrial natriuretic peptide (ANP) and urinary cyclic guanosine monophosphate (cGMP), in the healthy subjects (ANP P = 0.001, cGMP P = 0.043), which was not seen in the diabetic subjects (ANP P = 0.51, cGMP P = 0.74). Rosiglitazone restored the immersion-induced increase in cGMP excretion and rise of ANP in the diabetic group (ANP P = 0.048, cGMP P = 0.009). This study confirms that type 2 diabetic subjects have an impaired natriuretic response to acute volume expansion, which appears to be enhanced rather than diminished by rosiglitazone. This may be related to its effects in increasing natriuretic peptides and restoring the impaired cGMP excretion to volume expansion.

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