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Results for “Intracellular Fluid”

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PubMed1979

Volume studies in men with mild to moderate hypertension.

The importance of salt and water in the pathophysiology of the hypertensive state is well recognized. The current study is the first to report simultaneous measurements of red blood cell mass, plasma volume, extracellular fluid and total body water levels. Studies were performed in 82 white men, 14 with normal blood pressure and 16 with low renin and 52 with normal renin hypertension. The results indicate that subjects with normal renin hypertension compared with age-matched controls are characterized by an absolute increase (1.5 liter/m2) in intracellular fluid (total body water minus extracellular fluid). Furthermore, the ratio of extracellular fluid to total body water is decreased (0.43 to 0.38). No volume differences were found between subjects with low renin hypertension and age-matched subjects with normal renin hypertension. We conclude that subjects with normal renin hypertension compared with age-matched peers are characterized by an expanded intracellular fluid and that subjects with low renin hypertension do not exhibit a unique volume disorder.

Adult↗

PubMed1986

A pharmacological explanation of the use-dependency of the verapamil (and D-600) block of slow calcium channels.

Contractures of the toe muscles of frogs produced by 123 mM K+ were reduced or blocked by verapamil (or D-600) when applied in concentrations of 10(-7) M or more. In concentrations between 10(-7) and 3 X 10(-5) M or less, little or no reduction was produced in the first test with high K+ after drug application. When tests were repeated at 10- to 15-min intervals, block was produced. This block decreased and eventually disappeared if the muscles were kept in the drug solution without testing for 25 min or more. In contrast, at 10(-4) M verapamil, the first contracture in response to high K+ was reduced or blocked. If exposure to 10(-4) M verapamil was limited to 0.5 hr, then recovery occurred in drug-free solution, but if the muscles were exposed to this concentration of verapamil for 2.5 hr or longer, the K+ contracture remained blocked, even in drug-free solution. These results provided an explanation for the frequency- and use-dependency effects of verapamil and D-600. Briefly, this explanation is that the drug receptor is inside the calcium channel which is closed to the extracellular fluid in the resting or in the inactivated state but open to the intracellular fluid at all times. The drug receptors will be effectively occupied and a block produced when lower drug concentrations are used if the calcium channels are opened, but verapamil will leave its receptor and diffuse into the intracellular fluid when the extracellular channel openings are closed. Further details of this mechanism are given in the paper.

Animals↗

PubMed1999

Water and electrolyte shifts with partial fluid replacement during exercise.

In this study, we examined whether athletes, who typically replace only approximately 50% of their fluid losses during moderate-duration endurance exercise, should attempt to replace their Na+ losses to maintain extracellular fluid volume. Six male cyclists performed three 90-min rides at 65% of peak O2 uptake in a 32 degrees C environment and ingested either no fluid (NF), 1.21 of water (W), or saline (S) containing 100 mmol of NaCl x l(-1) to replace their electrolyte losses. Both W and S conditions decreased final heart rates by approximately 10 betas min(-1) (P<0.005) and reduced falls in plasma volume (PV) by approximately 4% (P<0.05). Maintenance of PV after 10 min in the W trial prevented further rises in plasma concentrations of Na+ [Na+], Cl- and protein but in the S and NF trials, plasma [Na+] continued to increase by approximately 4 mEq x l(-1). Differences in plasma [Na+] had little effect on the approximately 2.4 l fluid, approximately 120 mEq Na+ and approximately 50 mEq K+ losses in sweat and urine in the three trials. The main effects of W and S were on body fluid shifts. During the NF trial, PV and interstitial fluid (ISF) and intracellular fluid (ICF) volumes decreased by approximately 0.1, 1.2 and 1.0 l, respectively. In the W trial, the approximately 1.2 l fluid and approximately 120 mEq Na+ losses contracted the ISF volume, and in the S trial, ISF volume was maintained by the movement of water from the ICF. Since the W and S trials were equally effective in maintaining PV, Na+ ingestion may not be of much advantage to athletes who typically replace only approximately 50% of their fluid losses during competitive endurance exercise.

Adult↗

PubMed1999

Effect of prolonged restriction of motor activity on primates hydration homeostasis.

It has been assumed that restriction of motor activity (hypokinesia) induces significant changes in body hydration homeostasis. Thus, the objective of this study was to measure body hydration level during prolonged hypokinesia (HK). The studies were done on 12 male Macaca Mulatta (rhesus monkeys) aged three to five years (4.75 to 6.96 kg) during a 15-day period of pre HK and a 90-day period of HK. All primates were divided equally into two groups: monkeys placed under vivarium conditions served as vivarium control primates (VCP) and monkeys subjected to HK served as hypokinetic primates (HKP). For simulation of the HK effect, the HKM group was kept for 90 days in small individual cages that restricted their movements in all directions without hindering food and water intakes. During the pre HK period of 15 days and the HK period of 90 days the following parameters were measured: total body water (TBW), extracellular fluid volume (EFV), intracellular fluid volume (IFV), circulating plasma volume (CPV) and interstitial fluid volume (IsFV), urinary and plasma sodium and potassium, fluid consumption and elimination in urine, and body weight. Significant (p < or = 0.01) decrease in the TBW, IFV, and CPV was observed in the HKP group when compared with the VCP group. In the HKP group EFV and IsFV decreased significantly (p < or = 0.01) when compared with the VCP group only in the initial seven days of the HK period, while after the 7th day progressive increase could be observed. Fluid loss, urinary electrolyte excretion and plasma electrolyte concentration increased significantly (p < or = 0.01), while fluid intakes decreased significantly (p < or = 0.01) in the HKP group when compared with the VCP group. In the HKP group body weight decreased significantly (p < or = 0.01) when compared with the VCP group. In the VCP group the measured parameters did not change significantly when compared with the baseline control values. It was concluded that prolonged exposure to HK induces significant changes in body hydration homeostasis while body dehydration in monkeys caused primarily due to decreased CPV.

Animals↗

PubMed2001

Bioelectric impedance analysis of acute body water changes in congestive heart failure.

The body water changes indicated by bioelectric impedance analysis (BIA) and body weight were studied in 12 patients admitted to hospital for acute treatment of congestive heart failure (NYHA-class II-III). BIA was performed at the time of admittance and on the third day by using a multifrequency technique, which allows simultaneous estimation of the total body water (TBW) and the extracellular fluid (ECF) and intracellular fluid (ICF) volumes. The body weight at admittance was 85+/-20 kg. Body weight correlated with the body water compartments (r - 0.9, p<0.001). From day 1 to day 3, the body weight decreased by 2.9+/-1.7 kg. BIA estimated the corresponding reductions of the physiological body fluid spaces to 3.2+/-2.4 L (TBW), 2.7+/-1.6 L (ECF) and 0.5+/-3.2 L (ICF). These results indicate that diuretic treatment for acute congestive heart failure mainly lowers the ECF volume. However, changes in body weight correlated poorly with changes in TBW, r=-0.11. We conclude that, although BIA corresponded well to the weight changes at the group level, a poor correlation in individual patients suggests that BIA is not a suitable tool to monitor the fluid balance in patients with acute congestive heart failure undergoing diuretic treatment.

Aged↗

PubMed1989

Osmoregulation and body fluid compartmentalization in dehydrated heat-exposed pigeons.

Osmoregulatory and volume-regulatory responses of heat-acclimated pigeons (Columba livia) were studied during normal hydration and dehydration combined with heat exposure. Dehydrated heat-exposed pigeons (exposure to 50 degrees C following 48 h of water deprivation; 16-18% mass loss) could recover 97% of their initial body mass within 30 min of free drinking at the end of heat exposure. At the end of heat exposure, body temperature increased by 3 degrees C and hematocrit increased by 12.5%. Serum electrolyte and protein concentrations increased by 33-53% (P less than 0.001). Serum osmolality reached an outstanding mean value of 436.7 +/- 28.5 mosmol/kg (n = 11), 30.5% higher than the normal mean value. Serum glutamic-pyruvic transaminase and glutamic-oxaloacetic transaminase concentrations did not change during dehydration, suggesting no impairment in circulatory function. Blood urea nitrogen increased sixfold, indicating a total shutdown of the kidney. Relative plasma volume was maintained during dehydration at the expense of extravascular spaces and with a decreased vascular permeability as indicated by the increase in Evans blue-labeled albumin half-life (control, 104 +/- 53 min; dehydration, approaching infinity). Altogether, extracellular fluid volume and intracellular fluid volume contributed 53 and 47% of the evaporative water loss, respectively. It is concluded that plasma volume regulation may play an important role in the effective thermoregulatory responses of heat-exposed dehydrated pigeons. This regulation is achieved by preferential shifts of body water reserves among the various body water compartments coinciding with a remarkable tolerance to high osmotic pressures.

Acclimatization↗

PubMed1997

Effects of endurance training on the cardiovascular system and water compartments in elderly subjects.

The effects of endurance training on the water compartments and the cardiovascular system were determined in 10 elderly subjects [age 62 +/- 2 yr, pretraining maximal oxygen consumption (VO2 max)/kg = 25 +/- 2 ml . min-1 . kg-1 body wt]. They trained on a cycloergometer 3 times/wk for 16 wk (50-80% VO2 max, then 80-85% VO2 max). They were checked at 8 wk, 16 wk, and 4 mo after detraining. Training improved VO2 max (+16%) and induced plasma volume expansion (+11%). No change in total body water, extracellular fluid, interstitial and intracellular fluid volumes, fat-free mass, and body weight was detected in this small sample with training. Body fat mass decreased (-2.1 +/- 2.2 kg). Echocardiography at rest showed increased fractional shortening and ejection fraction and decreased left ventricular end-systolic dimension (P < 0.05). Blood volume expansion correlates with cardiac contractility and has an impact on cardiac function. These improvements are precarious, however, and are completely lost after 4 mo of detraining, when elderly subjects lose the constraints and the social stimulation of the imposed protocol.

Aged↗

PubMed1980

Properties of carnitine transport in rat kidney cortex slices.

The properties of carnitine transport were studied in rat kidney cortex slices. Tissue:medium concentration gradients of 7.9 for L-[methyl-14C]carnitine were attained after 60-min incubation at 37 degrees C in 40 microM substrate. L- and D-carnitine uptake showed saturability. The concentration curves appeared to consist of (1) a high-affinity component, and (2) a lower affinity site. When corrected for the latter components, the estimated Km for L-carnitine was 90 microM and V = 22 nmol/min per ml intracellular fluid; for D-carnitine, Km = 166 microM and V = 15 nmol/min per ml intracellular fluid. The system was stereospecific for L-carnitine. The uptake of L-carnitine was inhibited by (1) D-carnitine, gamma-butyrobetaine, and (2) acetyl-L-carnitine. gamma-Butyrobetaine and acetyl-L-carnitine were competitive inhibitors of L-carnitine uptake. Carnitine transport was not significantly reduced by choline, betaine, lysine or gamma-aminobutyric acid. Carnitine uptake was inhibited by 2,4-dinitrophenol, carbonyl cyanide m-chlorophenyl-hydrazone, N2 atmosphere, KCN, N -ethylmaleimide, low temperature (4 degrees C) and ouabain. Complete replacement of Na+ in the medium by Li+ reduced L- and D-carnitine uptake by 75 and 60%, respectively. Complete replacement of K+ or Ca2+ in the medium also significantly reduces carnitien uptake. Two roles for the carnitine transport system in kidney are proposed: (1) a renal tubule reabsorption system for the steady-state maintenance of plasma carnitine; and (2) maintenance of normal carnitine levels in kidney cells, which is required for fatty acid oxidation.

Acetylcarnitine↗

PubMedDate not supplied

Control of ventilation in the hypercapnic skate Raja ocellata: II. Cerebrospinal fluid and intracellular pH in the brain and other tissues.

This study examined the possible role(s) of central acid-base stimuli in the increase in ventilation induced by hypercapnia in the skate, a response that is not due to an O2 signal (Graham et al., Respir. Physiol., 1990, 80: 251-270). Skate were sampled for cerebrospinal fluid (CSF) acid-base status, intracellular pH of the brain (14C-DMO method), and pHi in other tissues throughout 24 h of exposure to PICO2 = 7.5 Torr. CSF PCO2 rapidly equilibrated with the elevated PaCO2. Despite the much lower non-HCO3- buffer capacity in the CSF, CSF pH was not depressed to the same extent as blood pHa. CSF pH was also regulated rapidly, returning to control levels by 8-10 h, whereas pHa remained significantly depressed at 24 h. Similarly, the pHis of the weakly buffered brain and heart ventricle were initially compensated more rapidly than those of more strongly buffered white muscle and red blood cells. However, brain pHi adjustment slowed markedly after 4 h and stabilized at only 70% compensation by 20-24 h, suggesting that brain intracellular acidosis may play a role in the long-term increase in ventilation. CSF and brain were the only compartments which did not exhibit an apparent compounding metabolic acidosis during the initial stages of hypercapnic exposure. While these results illustrate the primacy of central acid-base regulation, they do not support a role for CSF pH in the long-term elevation of ventilation in response to hypercapnia. Depressions in pHa and brain pHi appear the two most likely candidates for proximate stimuli.

Acid-Base Equilibrium↗

PubMedDate not supplied

Effects of prolonged acclimation to cold on the extra--and intracellular acid-base status in the land snail Helix lucorum (L.).

The aim of this study was to examine the effect of prolonged acclimation to cold on the acid-base status of extra- and intracellular fluids in the land snail Helix lucorum. For this purpose, acid-base parameters in the hemolymph and tissues were determined. In addition, the buffer values of hemolymph and tissues were determined in order to examine whether they change in the snails during acclimation to cold. According to the results presented, there is an inverse pH-temperature relationship in the hemolymph within the first day of acclimation, which is consistent with alphastat regulation. The Pco2 decreased, and pH in the hemolymph (pH(e)) increased by 0.32 U within the first day of acclimation to cold, which corresponds to a change of 0.013 U degrees C(-1). After the first day of acclimation, Pco2 increased in the hemolymph, resulting in a significant drop in pH(e) by 90 d of acclimation to cold. Acclimation of snails to low temperatures did not change the buffer value of the hemolymph. Also, intracellular pH (pH(i)) and intracellular buffer values remained stable during acclimation to cold for prolonged periods. The latter results in conjunction with those obtained by the in vitro determination of the passive component of intracellular fluids indicate an active regulation of pH(i) in H. lucorum during acclimation to cold.

Acclimatization↗

PubMedDate not supplied

Brain interstitial fluid and intracellular distribution of phenytoin.

After intravenous (i.v.) administration (10 mg/kg), the biodisposition of phenytoin (PHT) in serum (total and free concentration), cerebrospinal fluid (CSF), brain, and the interstitial fluid (IF) of the normal brain were determined in dogs. A sufficient volume of IF was obtained through a multiperforated polypropylene ball implanted into the left parietotemporal region for 4-5 weeks. PHT brain distribution coefficient values ranged between 1.9 and 3.75, while the ratios of IF to free serum PHT concentrations ranged between 0.19 and 1.04; thus, our data indicate that most of the free unbound PHT which enters the brain parenchyma accumulates in the cellular compartment. Furthermore, at 60 and 90 min the peak CSF and IF concentrations are delayed; thus, for PHT, an apparent diffusion front from the CSF into the extracellular space of the brain seems to occur.

Animals↗

PubMedDate not supplied

Colloid and crystalloid fluid resuscitation.

The choice of colloid or crystalloid solutions for fluid resuscitation of critically ill patients remains controversial. Marked reduction of extracellular water is considered an important defect in shock by proponents of crystalloid fluid therapy. Large volumes of crystalloid replenish this extracellular deficit. Hypovolemia is regarded as the primary defect in shock by those favoring colloid fluid therapy. Colloidal fluids promptly restore plasma volume and reestablish hemodynamic stability with substantially lesser volumes of fluid. However, only 8% of infused water and less than 25% of infused saline are retained in the intravascular fluid compartment after 1 h. On the other hand, almost the entire volume of iso-oncotic colloid is retained with the intravascular space after 1 h. Hypertonic saline decreases intracellular fluid volume. Hyperoncotic colloid decreases both interstitial and intracellular fluid volumes as it disproportionately expands intravascular volume. The choice of fluid is not only contingent on the restoration of intravascular volume, the rapidity with which it is accomplished and the duration of its effect, but also on the adverse effects that follow fluid resuscitation. This is of greatest moment in the fluid resuscitation of patients in whom circulatory shock follows volume depletion. Crystalloid fluid repletion which requires between 2- and 4-fold as much volume as colloidal fluid is of little risk in the young, traumatically injured patient. However, in older patients, the risk of pulmonary edema is increased.

Albumins↗

PubMedDate not supplied

Creatine supplementation and anterior compartment pressure during exercise in the heat in dehydrated men.

CONTEXT: Theoretically, the risk of compartment syndrome is increased during creatine monohydrate (CrM) supplementation because of intracellular fluid retention in muscle cells and the overall increased size of the muscle tissue. Whether this change in intracellular fluid is associated with an increase in anterior compartment pressure in the lower leg when subjects are under thermal stress is unknown. OBJECTIVE: To assess the influence of CrM on the resting and postexercise anterior compartment pressure of the lower leg in mildly to moderately dehydrated males exercising in the heat. DESIGN: Double-blind, randomized, crossover design. SETTING: Human Performance Laboratory. PATIENTS OR OTHER PARTICIPANTS: Eleven well-trained, non- heat-acclimated, healthy males (age = 22 +/- 2 years, height = 181.1 +/- 7 cm, mass = 78.4 +/- 4.2 kg, V(O2)max = 50.5 +/- 3.4 mL.kg(-1).min(-1)). INTERVENTION(S): Subjects were supplemented with 21.6 g/d of CrM or placebo for 7 days. On day 7, they performed 2 hours of submaximal exercise, alternating 30 minutes of walking with 30 minutes of cycling in the heat, resulting in approximately 2% dehydration. This was followed by an 80-minute heat tolerance test (temperature = 33.5 +/- 0.5 degrees C, humidity = 41.0 +/- 12%), which included 12 repetitions of a 3-minute walk (pace = 4.0 +/- 0.1 miles/h, intensity = 37.1 +/- 6.1% V(O2)max) alternating with a 1-minute, high-intensity run (pace = 11.8 +/- 0.4 miles/h, intensity = 115.0 +/- 5.6% V(O2)max), resulting in an additional 2% decrease in body weight. MAIN OUTCOME MEASURES: Before supplementation and on day 7 of supplementation, anterior compartment pressure was measured at rest, after dehydration, and at 1, 3, 5, 10, 15, and 60 minutes after the heat tolerance test. Analysis of variance with repeated measures was calculated to compare differences within the trials and time points and to identify any interaction between trial and time. RESULTS: The CrM intake was associated with an increase in body weight (P < .05). A moderate effect size was noted for compartment pressures between the trials for the differences between predehydration and postdehydration (eta2 = 0.414). This effect diminished substantially by 3 minutes after the heat tolerance test. Compared with the placebo trial, the change in anterior compartment pressure from rest to dehydration was greater, as was the change from rest to 1 minute after the heat tolerance test (P < .05) during the CrM trial. CONCLUSIONS: A 7-day loading dose of CrM increased anterior compartment pressures after dehydration and immediately after the heat tolerance tests, but the changes did not induce symptoms and the pressure changes were transient.

Journal Article↗

PubMed1990

In vivo measurement of intra- and extracellular space of brain tissue by electrical impedance method.

An impedance method was applied to evaluate transcellular fluid shifts in ischaemic brain oedema. The admittances (apparent electrical conductivities) of tissues were measured at varied frequencies based on a simple model of an electrical equivalent circuit for tissues, which consisted of Re (resistivity of extracellular fluid), Ri (resistivity of intracellular fluid) and Cm (capacitance of cell membrane). Calculated were Re, Ri, Rinf (resistivity of total fluid), Re/Ri and alpha (Cole-Cole distribution index) of brain tissue by Cole-Cole an arc of a circle. During ischaemia induced by cat middle cerebral artery occlusion (MCAO), the parameters were examined continuously. After MCAO, cerebral blood flow (CBF) decreased to under 10 ml/100 g/min. Then Re and Re/Ri increased, but Ri decreased. These results indicated that fluid shift from extracellular (EC) to intracellular (IC) space occurred after ischaemic insult. Rinf showed no changes during ischaemia of 30 min, which demonstrated no changes of total fluid volume. Using this impedance technique, fluid accumulation and shift may be examined by changes of Re, Ri, Re/Ri and Rinf in various types of brain oedema in vivo.

Animals↗

PubMed2001

Peak rates of diuresis in healthy humans during oral fluid overload.

OBJECTIVE: To determine whether rates of intestinal fluid absorption and renal diuresis can match high rates of fluid ingestion in healthy humans exposed to oral fluid overload, thereby preventing the development of hyponatraemia either by reverse sodium movement across the intestine (the Priestley-Haldane effect) or by expansion of the extracellular fluid volume. METHODS: Changes in renal function and in plasma chemical measurements in response to an oral fluid overload (0.9-1.8 l/h x 3 h) were investigated in 6 healthy control subjects at rest, and in a subject with a history of exercise-induced symptomatic hyponatraemia, during both prolonged (160-minute) exercise and at rest. FINDINGS: All control subjects gained weight (2.7 +/- 0.2 kg, mean +/- standard error of mean (SEM)) because the rate of oral fluid intake exceeded the peak rate of urine production (778 +/- 39 ml/h). Blood volume rose by 7.1 (+/- 0.5)% and plasma sodium concentrations fell progressively from 144 +/- 2.6 to 136 +/- 1.1 mmol/l (P < 0.05) in the control subjects. Plasma potassium and angiotensin II concentrations were unchanged and creatinine clearance was normal (approximately 125 ml/min). Free water clearance reached a maximum of 11.2 +/- 0.9 ml/min after 2 hours. The increase in body mass could be accounted for by calculated or measured changes in extra- and intracellular fluid volumes. Similar changes were measured in the subject with a previous history of symptomatic hyponatraemia. CONCLUSION: The rate of intestinal fluid absorption appeared to match the rate of oral fluid ingestion and there was no evidence of fluid accumulation in the intestine with reverse sodium movement from the extracellular space into intestinal fluid. The results of this study are therefore at variance with the Priestley-Haldane hypothesis and suggest that reverse sodium movement did not contribute to the hyponatraemia induced by oral fluid overload in these subjects. Rather it appears that humans may have a limited capacity to excrete fluid at rates in excess of approximately 900 ml/h in response to higher rates of oral fluid intake. When the rate of intestinal fluid absorption matches the rate of fluid ingestion and exceeds the kidneys' maximum capacity for fluid excretion, the excess fluid accumulates in the extra- and intracellular fluid compartments, inducing the dilutional hyponatraemia of water intoxication. These findings may have relevance to other clinical conditions in which hyponatraemia develops in response to high rates of oral or intravenous fluid provision.

Adult↗

PubMed1976

Transport of leucine and sodium in central nervous tissue: studies on retina in vitro.

Unidirectional leucine fluxes were measured in isolated rabbit retina maintained under steady state conditions in medium resembling CSF but with leucine varied from 2 to 20,000 microM. At physiological leucine concentration (11 microM), 1/2 time for outward transport was 88 s and intracellular fluid was cleared of isotopically labelled leucine at 2.3 ml/g dry wt./min; 1/2 time for inward transport was 16 s and interstitial fluid was cleared at 7.5 ml/g dry wt./min. The rate of leucine influx corresponded quite well with its rate of disappearance from the intracellular fluid, over a wide range of concentrations. Exchange diffusion was demonstrated for transport in both directions. There was competition by other amino acids, but no interaction between Na+ and leucine transport could be demonstrated. Kinetic analysis indicated the presence of more than one transport system for leucine. There was an unexpected fall in the efflux coefficient, with reduction in leucine concentration at the lower end of the concentration range, for which an explanation is proposed. Under control conditions, 1/2 time for efflux of intracellular 24Na+ was about 0.9 min. With intracellular Na+ increased 4 fold, 1/2 time for efflux was slightly reduced. Problems encountered in measuring fluxes in organized tissue are discussed.

Animals↗

PubMed1984

Ultrafiltration by hyperosmotic peritoneal dialysis fluid excludes intracellular solutes.

During peritoneal dialysis, progressive increments in the osmotic gradient increase ultrafiltration rate. Solute transport by convective flux is thereby raised but there is no preferential increase in potassium clearance. The data imply that ultrafiltrate derives from extracellular fluid alone. Mesothelial cells appear to resist solute and water flux in response to an immediately adjacent osmotic gradient.

Animals↗

PubMed1986

Simultaneous determination of fluid shifts during thermal stress in a small-animal model.

We have developed methodology to simultaneously measure fluid redistribution among the major compartments during moderate and severe hypohydration. Total body water (TBW) was determined using tritiated water, extracellular fluid volume (ECF) was measured using a single-injection [14C]inulin technique, and plasma volume (PV) was determined by indocyanine green dye dilution. Moderate (10% decrease in body wt) and severe (15%) hypohydration resulted in significant losses in TBW, ECF, and PV. Plasma volume was decreased by approximately 25% in both groups, and other fluid compartments were differentially affected. For example, the moderately dehydrated group maintained PV by shifting fluid from the interstitial fluid volume (ISF) compartment while preserving the intracellular fluid volume (ICF); conversely, the severely dehydrated group maintained PV by redistributing fluid from both the ISF and ICF compartments. The data indicated that the initial response to fluid loss was the movement of fluid from the ISF pool to sustain both PV and ICF. In severely hypohydrated rats, PV was maintained at the expense of ICF. These experiments indicated that PV and ICF were maximally protected, probably to preserve the integrity of the cardiovascular system and to minimize organ injury.

Animals↗