Time course and magnitude of changes in total body water, extracellular fluid volume, intracellular fluid volume and plasma volume during submaximal exercise and recovery in horses

2004 ◽  
Vol 1 (2) ◽  
pp. 131-139 ◽  
Author(s):  
Michael I Lindinger ◽  
Gloria McKeen ◽  
Gayle L Ecker

AbstractThe purpose of the present study was to determine the time course and magnitude of changes in extracellular and intracellular fluid volumes in relation to changes in total body water during prolonged submaximal exercise and recovery in horses. Seven horses were physically conditioned over a 2-month period and trained to trot on a treadmill. Total body water (TBW), extracellular fluid volume (ECFV) and plasma volume (PV) were measured at rest using indicator dilution techniques (D2O, thiocyanate and Evans Blue, respectively). Changes in TBW were assessed from measures of body mass, and changes in PV and ECFV were calculated from changes in plasma protein concentration. Horses exercised by trotting on a treadmill for 75–120 min incurred a 4.2% decrease in TBW. During exercise, the entire decrease in TBW (mean±standard error: 12.8±2.0 l at end of exercise) could be attributed to the decrease in ECFV (12.0±2.4 l at end of exercise), such that there was no change in intracellular fluid volume (ICFV; 0.9±2.4 l at end of exercise). PV decreased from 22.0±0.5 l at rest to 19.8±0.3 l at end of exercise and remained depressed (18–19 l) during the first 2 h of recovery. Recovery of fluid volumes after exercise was slow, and characterized by a further transient loss of ECFV (first 30 min of recovery) and a sustained increase in ICFV (between 0.5 and 3.5 h of recovery). Recovery of fluid volumes was complete by 13 h post exercise. It is concluded that prolonged submaximal exercise in horses favours net loss of fluid from the extracellular fluid compartment.

1963 ◽  
Vol 18 (6) ◽  
pp. 1231-1233 ◽  
Author(s):  
S. G. Srikantia ◽  
C. Gopalan

Determinations of body-fluid spaces with antipyrine for total-body water and sodium thiocyanate for extracellular fluid volume, hematological indices, and several serum constituents in about 500 Macaca radiata monkeys revealed that most of the values obtained were very similar to values obtained in man. body fluid spaces; hematology Submitted on April 22, 1963


2019 ◽  
pp. 04-13
Author(s):  
Colin Jones ◽  
Louise Wells ◽  
Graham Woodrow ◽  
David Ashford

Background: Metabolic acidosis in chronic kidney disease (CKD) is often treated with oral sodium bicarbonate. There is limited evidence around the effects of sodium bicarbonate on extracellular fluid and blood pressure in CKD. Methods: In a double blind randomised comparison patients with stage 3-5 CKD were randomised to either oral sodium bicarbonate 1.5 g three times a day (n=18) or placebo (n=21) for 4 weeks. Assessments performed at 0 and 4 weeks included: body weight, office blood pressure and assessment for peripheral/pulmonary oedema; serum creatinine, electrolytes and venous bicarbonate; 24-hour urine for sodium excretion; extracellular fluid volume and total body water determined by sodium bromide and deuterium oxide dilution respectively; extracellular fluid volume and total body water by bioimpedance. Differences between the active and placebo groups at week 4 were analysed by ANCOVA. Results: At week 4, serum bicarbonate was higher (25.6±2.4 vs 23.3±3.1 mmol/l) and blood urea lower (14.2±5.6 vs 17.0±5.8 mmol/l) in the active treatment group. Urine sodium concentration was also higher (82.7±25.3 vs 59.0±21.9 mmol/l). Extracellular fluid volume (20.0±4.3 vs 18.0±2.9) and total body water (42.3±9.6 vs 39.0±6.8) measured by bioimpedance and total body water by deuterium dilution (41.7±8.3 vs 39.4±6.2) were significantly greater in the treatment arm at week 4. Differences in systolic and diastolic blood pressure did not reach statistical significance. Conclusions: Oral sodium bicarbonate has a biological effect and increases body water content, without evidence of a clinical consequence. This may reflect the fact that some of the ingested sodium is excreted in the urine.


1982 ◽  
Vol 62 (1) ◽  
pp. 43-49 ◽  
Author(s):  
J. H. Bauer ◽  
C. S. Brooks

1. Erythrocyte mass, plasma volume (PV), extracellular fluid volume (ECFV) and total body water were simultaneously measured in 30 normotensive and 30 normal-renin hypertensive Caucasian male subjects for accurate determination of the presence or absence of a disorder(s) in body-fluid composition in hypertension. 2. The results indicate that plasma volume and total blood volume are lower in hypertensive subjects than in normotensive control subjects. The PV comprised 19% of the ECFV in both control and hypertensive subjects. 3. ECFV was lower in hypertensive subjects than in normotensive control subjects; the PV and interstitial fluid components of the ECFV were reduced by similar proportions. The ECFV, furthermore, comprised a smaller portion of the total body water in hypertensive subjects than that in control subjects. 4. We conclude that in the hypertensive state there is a reduction in the ECFV, but that there is no change in the partition of the ECFV between the plasma and interstitial components.


1983 ◽  
Vol 245 (6) ◽  
pp. R901-R905 ◽  
Author(s):  
S. L. Bealer ◽  
E. G. Schneider

The effects of electrolytic ablation of the periventricular tissue surrounding the anteroventral third ventricle (AV3V) of the rat brain on body fluid distribution and the renin-aldosterone system were determined. Rats underwent either ablation of AV3V periventricular tissue or control surgeries. After recovery, animals were implanted with femoral arterial and jugular venous catheters, and sodium space and plasma volume were measured by calculating the dilution of intravenous injections of 22Na- and 125I-labeled serum albumin, respectively. Total body water was determined in separate groups of rats by desiccation. Other animals with AV3V lesions and control rats were used to measure urinary sodium excretion and plasma renin (Prenin) and aldosterone (Paldo) concentrations while volume replete and after volume depletion. Animals with AV3V lesions had expanded extracellular fluid volume and decreased plasma volume, but total body water was comparable with control-operated rats. Volume-replete and volume-depleted rats with AV3V lesions had significantly higher Prenin than control animals in similar volume states. Although Paldo was not different between groups in the volume-replete state, it was significantly greater in rats with AV3V lesions than in control animals after volume depletion. These data demonstrate that AV3V periventricular ablation results in chronic alterations in the normal body fluid distribution but does not diminish the rats' ability to increase Prenin and Paldo or decrease sodium excretion during volume depletion.


1972 ◽  
Vol 43 (1) ◽  
pp. 79-90 ◽  
Author(s):  
F. Skrabal ◽  
R. N. Arnot ◽  
G. F. Joplin ◽  
T. R. Fraser

1. Simultaneous measurements of exchangeable Na+, exchangeable K+, extracellular fluid volume and total body water, with 24Na, 43K, 77Br and 3H2O, were carried out in patients with adrenocortical insufficiency due to pituitary ablation performed 1–3 months previously. 2. The first group of five patients was studied before and after withdrawal of maintenance prednisone (2·5 mg three times daily, orally). The effects of glucocorticoid withdrawal were: (a) an increase in intracellular water (all cases) and a decrease in the extracellular fluid volume (four cases) irrespective of any change in serum Na+ concentration; (b) an increase in residual (‘intracellular’) Na+ in all cases which was matched by a loss of extracellular Na+, so that total body Na+ remained unchanged, and (c) the cortisol deficiency clinical syndrome. Exchangeable K+ remained unchanged. 3. Similar measurements were obtained with two further patients during the corticosteroid withdrawal period, throughout which they were kept on a maintenance dose of deoxycorticosterone acetate, 1·0 mg twice daily sublingually. Neither the above biochemical changes nor the cortisol deficiency syndrome developed. 4. The shift into the cells of water and Na+ may depend on the same defect caused by glucocorticoid deficiency, and may be the cause of the cortisol deficiency syndrome.


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