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Studies on the interaction of regulatory mechanisms of body temperature, circulation and body fluid.

体温、循环、体液调节机制相互作用的研究。

基本信息

批准号：
62440026
负责人：
MORIMOTO Taketoshi
金额：
$ 11.46万
依托单位：
Kyoto Prefectural University of Medicine
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (A)
财政年份：
1987
资助国家：
日本
起止时间：
1987 至 1988
项目状态：
已结题

项目摘要

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.

热应激引起皮肤血管舒张和热脱水。在这种情况下的调节反应进行了研究，重点补液过程和控制的中心静脉压。在人类受试者中，通过饮酒的汗液损失的替代通常低于汗液损失，这种现象被称为自愿脱水在这个实验中，我们明确指出，这种脱水是由于体液的渗透稀释和损失的完全恢复，需要补充损失的盐。此外，我们表明，能够取代大鼠热脱水的NaCl浓度为0.2%至0.9%。当允许大鼠选择氯化钠溶液时，先摄入约50 meq/l的氯化钠溶液约2小时，然后再摄入约120 meq/l的氯化钠溶液，用犬和大鼠分析了对控静脉压（CVP）的调节机制：在犬，交感神经系统参与了对控静脉压的调节。CVP也参与了犬饮水行为的终止。采用热习服大鼠，观察热暴露期间血管顺应性的降低。使用具有不同水合水平的大鼠，显示了来自CVP的总外周血管阻力的反馈控制。在此基础上，通过连续监测大鼠运动时循环血容量的变化和血钠、钾浓度的变化，可以揭示热应激时循环反应与血容量或体液调节的相互作用。