1988 Fiscal Year Final Research Report Summary
Studies on the interaction of regulatory mechanisms of body temperature, circulation and body fluid.
| Project/Area Number |
62440026
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| Research Category |
Grant-in-Aid for General Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
環境生理学(含体力医学･栄養生理学)
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
MORIMOTO Taketoshi Kyoto Prefectural University of Medicine, Professor, 医学部, 教授 (30079694)
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| Co-Investigator(Kenkyū-buntansha) |
ITOH Toshiyuki Kyoto Prefectural University of Medicine, Instructor, 医学部, 助手 (90168360)
NAKAI Mikio Kyoto Prefectural University of Medicine, Instructor, 医学部, 助手 (60201662)
NOSE Hiroshi Kyoto Prefectural University of Medicine, Assistant Professor, 医学部, 講師 (40128715)
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| Project Period (FY) |
1987 – 1988
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| Keywords | Heat stress / Blood volume / Vascular compliance / Central venous pressure / Fluid intake / 循環血液量 / 飲水行動 |
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| Research Abstract |
Heat stress causes cutaneous vasodilation and thermal dehydration. Regulatory responses under this condition were studied focusing rehydration process and control of central venous pressure.
In human subjects, the replacement of sweat loss by drinking is usually lower than sweat loss, and the phenomenon is known as voluntary dehydration in this experiment we made it clear that this dehydration is due to osmotic dilution of body fluid and for the full restitution of the loss, replacement of lost salt is required. In addition, we showed that NaCl concentration which enable to replace thermal dehydration in rats was from 0.2 to 0.9% when provided alone. When rats were allowed to choose NaCl solution, about 50 meq/l of NaCl solution was taken for about 2 hours and then that of about 120 meq/l was consumed.
The regulatory mechanism of contral venous pressure (CVP) was analyzed using dogs and rats: The involvement of sympathetic nervous system in the regulation of CVP was shown in dogs by total spinal block and adrenergic agonist. The involvement of CVP in the termination of drinking behavior was also shown in dog. Using heat acclimatized rats, lowering of vascular compliance during heat exposure was observed. Using rats with different hydration levels, feedback control of total peripheral vascular resistance from CVP was shown. In addition to these experiments, the changes in circulating blood volume was monitored continuously together with the change in blood sodium and potassium concentration during exercise in rats.
Based on these results, it became possible to depict the interaction between circulatory responses and blood volume or body fluid regulation under heat stress.
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