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Physiologic mechanisms of circulatory and body fluid losses in weightlessness identified by mathematical modeling

Author
Srinivasan, R. S.
Published
Feb 1, 1993.
Physical Description
1 electronic document
Additional Creators
Charles, J. B. and Simanonok, K. E.
Online Version

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Summary
Central volume expansion due to fluid shifts in weightlessness is believed to activate adaptive reflexes which ultimately result in a reduction of the total circulating blood volume. However, the flight data suggests that a central volume overdistention does not persist, in which case some other factor or factors must be responsible for body fluid losses. We used a computer simulation to test the hypothesis that factors other than central volume overdistention are involved in the loss of blood volume and other body fluid volumes observed in weightlessness and in weightless simulations. Additionally, the simulation was used to identify these factors. The results predict that atrial volumes and pressures return to their prebedrest baseline values within the first day of exposure to head down tilt (HDT) as the blood volume is reduced by an elevated urine formation. They indicate that the mechanisms for large and prolonged body fluid losses in weightlessness is red cell hemoconcentration that elevates blood viscosity and peripheral resistance, thereby lowering capillary pressure. This causes a prolonged alteration of the balance of Starling forces, depressing the extracellular fluid volume until the hematocrit is returned to normal through a reduction of the red cell mass, which also allows some restoration of the plasma volume. We conclude that the red cell mass becomes the physiologic driver for a large 'undershoot' of the body fluid volumes after the normalization of atrial volumes and pressures.
Other Subject(s)
Collection
NASA Technical Reports Server (NTRS) Collection.
Note
Document ID: 19940007085.
Accession ID: 94N11557.
NASA. Johnson Space Center, Sixth Annual Workshop on Space Operations Applications and Research (SOAR 1992), Volume 2; p 598-604.
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No Copyright.
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