Our purpose was 1) to test the hypothesis that in man there is a range of plasma osmolality within which the red cell volume (RCV) and mean corpuscular volume (MCV) remain essentially constant and 2) to determine the upper limit of this range. During a variety of stresses--submaximal and maximal exercise, heat and altitude exposure, +Gz acceleration, and tilting--changes in plasma osmolality between -1 and +13 mosmol/kg resulted in essentially no change in the regression of percent change in plasma volume (PV) calculated from a change in hematocrit (Hct) on that calculated from a change in Hct + hemoglobin (Hb), i.e., the RCV and MCV were constant. Factors that do not influence RCV are the level of metabolism, heat exposure at rest, and short-term orthostasis (heat-to-foot acceleration). Factors that may influence RCV are exposure to high altitude and long-term orthostasis (head-up tilting). Factors that definitely influence RCV are prior dehydration and extended (greater than 2 h) periods of stress. Thus, either the Hct or the Hct + Hb equations can be used to calculate percent changes in PV under short-term (less than 2 h) periods of stress when the change in plasma osmolality is less than 13 mosmol/kg.

No abstract

The mass density of antecubital venous blood was measured continuously for 80 min/session with 0.1 g/l precision at a flow rate of 1.5 ml/min in six male subjects. Each person participated in two different sessions with the same protocol. To induce transvascular fluid shifts, the subjects changed from sitting to standing and from standing to supine positions. There was transient blood density shifts immediately after postural changes, followed by an asymptotic approach to a new steady-state blood density level. Additional deviations from a simple time course were regularly observed. Blood density increased by 3.5 +/- 1.4 (SD) g/l when standing after sitting and decreased by 5.0 +/- 1.2 g/l while supine after standing. The corresponding half time of the blood density increase was 5.6 +/- 1.4 min (standing after sitting) and 6.9 +/- 3.1 min (supine after standing) of the blood density decrease. Erythrocyte density was calculated and did not change with body position. Whole-body blood density was calculated from plasma density, hematocrit, and erythrocyte density, assuming an F-cell ratio of 0.91. Volume shifts were computed from the density data; the subject's blood volume density decreased by 6.2 +/- 1.2% from sitting to standing and increased by 8.5 +/- 2.1% from standing to supine. Additional discrete plasma density and hematocrit measurements gave linear relations (P less than 0.001) between all possible combinations of blood density, plasma density, and hematocrit.(ABSTRACT TRUNCATED AT 250 WORDS)

Indices of plasma hypertonicity, elevated plasma concentrations of solutes that draw fluid out of cells by osmosis, are needed to pursue hypertonicity as a possible risk factor for obesity and chronic disease. This paper proposes a new index that may be more sensitive to mild hypertonicity in vivo at a point in time than traditional measures. The index compares mean corpuscular volume (MCV) estimates from diluted (in solution by automated cell counter) and nondiluted blood (calculated from manual hematocrit, MCV ¼ Hct/RBC*10 6 ). A larger Auto vs Manual MCV (42 fl) in vitro indicates hypertonicity in vivo if the cell counter diluent is isotonic with the threshold for plasma vasopressin (PVP) release and PVP is detectable in plasma (40.5 pg/ml). To evaluate this principle of concept, hypertonicity was induced by 24-h fluid restriction after a 20 ml/kg water load in four healthy men (20-46 years). Unlike serum and urine indices, the MCV difference-&-PVP index detected hypertonicity in all participants.

The purpose was to determine whether extracellular volume or osmolality was the major contributing factor for reduction of thirst in air and head-out water immersion in hypohydrated subjects. Eight males (19-25 yr) were subjected to thermoneutral immersion and thermoneutral air under two hydration conditions without further drinking: euhydration in water (Eu-H2O) and euhydration in air, and hypohydration in water (Hypo-H2O) and hypohydration in air (3.7% wt loss after exercise in heat). The increased thirst sensation with Hypo-H2O decreased (P < 0.05) within 10 min of immersion and continued thereafter. Mean plasma osmolality (288 +/- 1 mosmol/kgH2O) and sodium (140 +/- 1 meq/l) remained elevated, and plasma volume increased by 4.2 +/- 1.0% (P < 0.05) throughout Hypo-H2O. A sustained increase (P < 0.05) in stroke volume accompanied the prompt and sustained decrease in plasma renin activity and sustained increase (P < 0.05) in plasma atrial natriuretic peptide during Eu-H2O and Hypo-H2O. Plasma vasopressin decreased from 5.3 +/- 0.7 to 2.9 +/- 0.5 pg/ml (P < 0.05) during Hypo-H2O but was unchanged in Eu-H2O. These findings suggest a sustained stimulation of the atrial baroreceptors and reduction of a dipsogenic stimulus without major alterations of extracellular osmolality in Hypo-H2O. Thus it appears that vascular volume-induced stimuli of cardiopulmonary baroreceptors play a more important role than extracellular osmolality in reducing thirst sensations during immersion in hypohydrated subjects.

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The present study determines the effect of repeated 70 degrees head-up tilt (HUT) on plasma volume (PV) shifts by measuring blood density (BD), plasma density (PD), and hematocrit (Hct). Eight men (18-26 yr) underwent a predrink period with two supine (P1 and P3) and two HUT (P2 and P4) phases of 45 min each. At the end of P4 they drank 10 ml/kg body wt of isotonic (290 mosmol/kg) sodium chloride (Iso) or hypotonic (< 10 mosmol/kg) unsweetened tea (Hypo) or nothing [control (Con)]. The following periods continued the supine (P5, P7)/upright (P6) sequence. BD and PD were measured from ear lobe blood; they were different (P < 0.05) between Con, Hypo, and Iso P6 and P7. The density of fluid that moved between intra- and extravascular compartments was 1,008.2 +/- 0.4 g/l and did not differ with test situations. In Con (P3, P5, P7), supine PV steadily decreased compared with P1 (P < 0.05). PV in P1, P2, and P3 of all treatments averaged 120 +/- 1, 101 +/- 1, and 115 +/- 1%, respectively, of PV in P4. Tilt-induced PV shifts ranged from -9.7 to -16.7% compared with PV during the respective previous phases. After drinking, PV increased (P < 0.05) above Con values at the end of P7 by 12.9% with Iso and by 6.6% with Hypo. Progressive hemoconcentration occurred in the nondrink supine periods; isotonic saline ingestion increased supine PV to Con level but did not stop or reverse the decrease of upright hemoconcentration.(ABSTRACT TRUNCATED AT 250 WORDS)

The influence of intravenous infusions of various concentrations of NaCl solutions on temperature regulation was investigated in dogs at rest and during moderate exercise for 1 h on a treadmill. Infusion of hypertonic solutions either before and during exercise resulted in elevated (P less than 0.05) plasma Na+ and osmotic concentrations and produced higher equilibrium levels (P less than 0.05) of rectal temperature (Tre) during exercise (prehypertonic 40.9 degrees C vs. no infusion 40.4 degrees C; hypertonic 40.8 degrees C vs. isotonic infusion 40.4 degrees C), but not at rest. Increasing the [Na+] and osmotic concentrations above 170 meq/liter and 325 mosmol/kg, respectively, resulted in no additional increase in exercise Tre. Water consumption during exercise decreased (P less than 0.05) plasma [Na+], osmolality, and the equilibrium level of Tre to control levels. There was no effect of changes in plasma volume (PV) of +/- 8% on the time course, equilibrium level, or change in Tre during exercise. At the end of exercise, there were moderate correlations (P less than 0.01) between Tre and [Na+] (r = 0.51) and Tre and osmoti (r = 0.52) concentrations. It was concluded that a) the exercise Tre responses of the dog respond quantitatively like man to elevated plasma [Na+] and osmolality, b) the Tre levels are not influenced by changes in PV, and c) water intake significantly reduces the ion-osmotic hyperthermia.