Intravascular and extracellular volumes in the diabetic rat
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Alloxan
Microdialysis
Interstitial fluid
Basal (medicine)
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Pathogenesis
Intracellular Fluid
Compartment (ship)
Primary (astronomy)
Homeostasis
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Dogs partially depleted of extracellular electrolytes by intraperitoneal glucose injections and then maintained on a salt-free diet showed absence of fluid intake and a negative water balance while the intracellular volumes were above normal. When these volumes had been reduced to stable minimal levels, water was taken by mouth and the negative water balance corrected. Although the intakes now rose to polydipsic levels, a positive balance was not established despite the fact that the extracellular volumes were still reduced. Intracellular volumes were not restored to the preëxperi-mental level. When NaCl was given, extracellular electrolytes and volumes were restored toward normal. The initial response was an increased intake which, however, was not sustained. The intracellular compartment, originally decreased, showed a delayed rehydration to normal levels. Hence the voluntary water intake showed more positive correlation with changes in intracellular volume than with extracellular volume change. Fluid balance was affected both by intracellular hydration and electrolyte levels in the extracellular fluid.
Intracellular Fluid
Body water
Fluid compartments
Water intake
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Intracellular pH
Extracellular polysaccharide
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Medulla
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1. The effects of pentobarbitone sodium (Nembutal) anaesthesia in dogs on extracellular fluid and plasma volumes, plasma protein concentration, haematocrit and extracellular fluid electrolyte composition were measured. 2. Induction of pentobarbitone anaesthesia caused a rapid rise in extracellular fluid volume, accompanied by decreases in the haematocrit, in extracellular fluid potassium concentration, and in plasma calcium, magnesium, and protein concentrations. There were no significant changes in plasma osmolality and extracellular fluid concentrations of sodium and chloride. 3. Extracellular fluid volume did not alter significantly during six hours of anaesthesia, but the haematocrit and extracellular fluid potassium concentration showed an increase towards control values. 4. The relevance of these findings to the interpretation of experiments carried out under pentobarbitone anaesthesia is noted.
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We have measured, directly and simultaneously, changes in extracellular volume and intra- and extracellular pH during ischemia in the isolated rat heart using 31P NMR spectroscopy. Hearts were perfused with buffer containing 15 mM sodium phenylphosphonate at pH 7.4. Wash in and wash out experiments showed that phenylphosphonate entered only the extracellular (interstitial, vascular and chamber) space of the heart and had no adverse effects on myocardial energetics, contractile function or coronary flow rate. Hearts were subjected to 28 min of total, global ischemia, during which the phenylphosphonate resonance area in the 31P NMR spectra decreased by 83%, indicating that extracellular fluid had moved rapidly from the heart to the bath surrounding the heart, partly as a result of vascular collapse. A separate, morphological study confirmed that 95% of the vasculature had collapsed by 28 min ischemia. Intra- and extracellular pH were determined from the chemical shifts of the P(i) and the phenylphosphonate resonances, respectively. In the pre-ischemic rat heart, intracellular pH was 7.15 +/- 0.03 and extracellular pH was 7.39 +/- 0.03. By 4 min of ischemia, intra- and extracellular pH were the same and decreased concomitantly throughout the remainder of ischemia to final values of 6.09 +/- 0.19 and 6.16 +/- 0.23, respectively. On reperfusion, the extracellular volume and pH returned to pre-ischemic levels within 1 min, but restoration of intracellular pH took > 2.5 min. Thus, a large volume of extracellular fluid moves out of the rat heart to the surrounding bath and the intra- and extracellular pH become the same during total, global ischemia.
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The purpose of this study was to determine the effect on cell survival of extracellular changes that occur during ischemia, over and above the depletion of O2 and substrate. Rabbit retinas were deprived in vitro of both O2 and substrate, and then returned to control medium for 4 h before recovery was assessed by measuring protein synthesis, glucose utilization, and tissue water. Experimental conditions were altered in various ways during the period of O2 and substrate deprivation in order to modify the changes taking place in the interstitial fluid as a result of the failure of energy metabolism. When O2-free, substrate-free extracellular electrolyte solution was added to the retinas to reduce the ischemia-induced changes in the interstitial fluid, there was marked reduction in irreversible damage. But when energy-deprived retinas were exposed to retinas that had already been ischemic, or to interstitial fluid from ischemic retinas, there was an increase in irreversible damage. Removing Ca++ from the extracellular fluid during the period of energy deprivation increased the damage due to short deprivations in a restricted volume of extracellular fluid, but reduced the damage from longer deprivations in a large volume of extracellular fluid. The results demonstrate that several changes occur in the extracellular fluid during ischemia that significantly affect recovery.
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hirst is a subjective perception that provides the urge for humans and animals to drink fluids. It is a component of the regulatory mechanisms that maintain body fluid homeostasis and ultimately is essential for survival. This urge to ingest fluids may arise for several reasons that include habitual, cultural, and psychogenic drives as well as the regulatory response to reductions in the fluid content of various bodily compartments, hypertonicity of the extracellular fluid, or increases in the circulating concentration of some dipsogenic hormones. Such regulatory thirst, and the cerebral mechanisms generating it, are the subjects of this review. When the body loses water, it is usually depleted from both the extracellular and intracellular compartments, but it may not necessarily be lost equally from each of the fluid spaces. Loss of NaCl (the major solute of the extracellular fluid) together with water results in proportionately more extracellular fluid being depleted than if water alone is lost. This may occur, for example, with fluid loss from the alimentary tract that occurs in conditions of vomiting or diarrhea, and when this fluid loss takes the form of an isotonic fluid, then the depletion will be entirely from the extracellular fluid. However, if hypertonic fluid is added to the extracellular compartment, there will be an osmotic depletion of water from the intracellular compartment into the extracellular fluid, and this latter compartment will be expanded. A range of compensatory responses are engaged when depletion of either the intra- or extracellular compartment occurs. These responses (e.g., vasopressin secretion, stimulation of the renin-angiotensin-aldosterone system, sympathetic activation, and reduced renal solute and water excretion) have the effect of minimizing changes in body fluid volume and composition. However, such mechanisms, although of undoubted benefit to the animal, do not restore body fluids to the original state. For this to occur, fluid losses must be replenished. Therefore, thirst, which provides the motivation to drink, is an important component of the coordinated sequence of physiological responses that maintain the volume and composition of body fluids. In the following paragraphs, we outline the cerebral mechanisms that subserve the water-drinking responses that are associated with 1) hypertonicity, cellular dehydration, and osmoreceptor stimulation; 2) hypovolemia and extracellular dehydration, including the role of circulating angiotensin (ANG) II as a dipsogenic hormone and the afferent neural inflow that also provides stimuli to the thirst mechanism; and 3) other hormonal signals that may stimulate (e.g., relaxin) or inhibit [e.g., atrial natriuretic peptide (ANP)] thirst.
Intracellular Fluid
Fluid compartments
Compartment (ship)
Homeostasis
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1. A new technique is presented for determining the volume of extracellular space in bowfin (Amia calva) brain during in vitro incubation. It consists of solving simultaneous equations which are applied to determine the volume of extracellular space as well as intracellular marker concentration. This technique allows for a better insight into the redistribution of marker between incubation medium and extracellular space as well as between extracellular and intracellular space.2. Na(+), K(+) and Cl(-) equilibrated within 10-15 min between incubation medium and extracellular space. There was no evidence of a homoeostatic mechanism controlling the concentration of these ions in the extracellular fluid, which appeared to be in equilibrium with cerebrospinal fluid. The extracellular spaces of these ions were identical: Na(+), 23.4; K(+), 23.3 and Cl(-), 23.2%.3. Sorbitol equilibrated with the extracellular fluid within 45 min and indicated an extracellular space of 22.6%, nearly identical with that for electrolytes.4. Vastly different ;spaces' were obtained for [(3)H]methoxy inulin, which equilibrated within 45 min with a 13% space and [(14)C]carboxyl inulin, which showed a 46% space value for only 30 min. The difference may be explained by marker decomposition. The 9% difference between the [(3)H]methoxy inulin and sorbitol spaces may be explained by a ;packing' factor attributable to molecular size.
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