| Project/Area Number |
62570707
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
麻酔学
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| Research Institution | Department of Anesthesiology, Kyoto Prefectural University of Medicine |
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Principal Investigator |
OKUDA Chieko Department of Anesthesiology, Kyoto Prefectural University of Medicine, 医学部, 講師 (70079937)
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| Project Period (FY) |
1987 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1988: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1987: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | Circulatory Shock / Neuroactive Substances / Push-pull perfusion / Intracerebral Perfusion / thyrotropin-releasing hormone(TRH) / pushーpull perfusion / thyrotropinーreleasing hormone(TRH) / 脳環流 / thyrotropir-releasing hormone(TRH) |
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| Research Abstract |
In the early stage of circulatory shock, sympathetic reflexes and hormonal factors are known to compensate to prevent deterioration of the circulation. However, the central nervous system(CNS) mechanisms that mediate and coordinate such responses are largely unknown. This study is designed to identify the substance(s) in the brain, which are involved in central regulation of cardiovascular system during circulatory shock. I have studied the changes of brain thyrotropin-releasing hormone(TRH), as one of the candidates of such substances, released in the fourth ventricle of conscious rat after bleeding using a push-pull perfusion method. Centrally administered TRH is known to have the cardiovascular effect independent of its pituitary actions. In this study,it has been revealed that; 1) The concentration of TRH in the perfusate remained constant during the 140 min perfusion period in the control rat. 2) It was significantly increased during the first 20 min of perfusion immediately after withdrawing of 30% of the estimated total blood and it soon returned to the initial level. 3) Administration of neither normal rabbit serum nor antiserum of TRH into the ventricle had any significant effects on blood pressure or heart rate for 3 hr in the control animal. 4) After bleeding, animals that received TRH-antiserum showed a significantly greater decrease in blood pressure and longer duration of this decreased level than animals that received normal rabbit serum. The tendency of tachycardia which was seen immediately after bleeding in the latter animals was suppressed in the former animals, but no significant changes were detected. These results suggest that endogenous brain TRH is involved in the central regulation of the cardiovascular system after bleeding in conscious rats. However, it does not have any significant role in the central cardiovascular regulation in the normal state.
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