| Co-Investigator(Kenkyū-buntansha) |
HASHIMOTO Satoru Kyoto Prefectural University of Medicine, Dept. of Assistant, 医学部, 助手 (90167578)
HOSOKAWA Toyoshi Kyoto Prefectural University of Medicine, Dept. of Assist. Prof., 医学部, 講師 (80165555)
OKUDA Chieko Kyoto Prefectural University of Medicine, Dept. of Assist. Prof., 医学部, 講師 (70079937)
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| Research Abstract |
1. The purpose of the research The problems related to brain death and following organ transplantation are the states of other organs such as heart, kidney, liver, and endocrine and metabolic systems. Decision of brain death itself must be resurveyed from the stand point of brain metabolism and endocrine activity. If multiple organ failure occurred with brain death, transplantation of such failured organ will be meaningless. Investigation of shock organ, development of MOF,and brain endocrine system and metabolism during pre&ih brain death is the purpose of this project.
2. Results (1) Quantitative evaluation of irreversibility of shock Quantitative evaluation of irreversibility of shock in each organs and systems were done by animal experiments and clinical survey of shock cases. Quantitative representation is shown on each categories and indices such as clinical circulatory system, myocardial functions, blood gases, acid-base balances, metabolism, electrolytes, endocrine systems, and
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reticuloendotlierial system. Those figures are displayed on the table, and this will be very useful indices to evaluate the status of each organs and whole body condition. (2) Studies on reversibility and irreversibility of each organs, such as brain, heart, and kidney The effects of ischemia and postischemic reperfusion on brain cholinergic system of the rat and the effects of hyperoxia on central cholinergic system were investigated measuring activities of choline acetyltransferase, ACHE, and muscarinic ACh receptor. Suppression by ischemia and increase by hyperoxia were noted. Thyrotropin-releasing hormone (TRH) was investigated in detail on its cardiovascular effects and the role in hemorrhagic and endotoxin shock. The mechanism of its actions is summarized as follows. (1) The cardiovascular stimulating actions induced by centrally administered TRH are increase of sympathetic stimulation. (2) Presser effects of TRH are biptiasic and fast and continuous effects were noted. (3) Cholinergic, GABAergic, and dopaminergic central pathways are involved in the Presser action of TRH. (4) TRH increased in septum after hemorrhage, and high concentration of K increase TRH release dose-dependently. Stimulation of hemorrhage causes membrane depolarization of TRH contained nerve terminal and thus release of TRH increases. The effects of PGI_2 on coronary circulation in cardiogenic shock was studied together with the effect of PGE_1. Effect of arterial hypotension on canine circulating blood volume was calculated. The effects of nifedipine, nicardipine, ATP, and dichloroacetate on ischemic kidney were examined and their various effects were measured on renal blood flow and renal functions. Immunological and aminoacids measurement were also done to define reversibility. Less
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