1987 Fiscal Year Final Research Report Summary
Expoloration of spasmogenic factors and its antagonist for cerebrovasculor spasm
| Project/Area Number |
60870010
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| Research Category |
Grant-in-Aid for Developmental Scientific Research
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| Allocation Type | Single-year Grants |
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| Research Field |
General pharmacology
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| Research Institution | Kyoto University |
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Principal Investigator |
FUJIWARA Motohatsu Department of Pharmacology, Faculty of Medicine, 医学部, 教授 (90025536)
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| Co-Investigator(Kenkyū-buntansha) |
OKAMOTO Shinichiro Department of Neurosurgery, Faculty of Medicine, 医学部, 助手 (40160717)
MIWA Soichi Same to above, 医学部, 助手 (40157706)
TANIGUCHI Takashi Same to above, 医学部, 講師 (10111957)
NARUMIYA Shu Department of Pharmacology, Faculty of Medicine, 医学部, 助教授 (70144350)
KURAHASHI Kazuyoshi Radioisotope Research Center, 放射性同位元素総合センター, 助教授 (10025653)
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| Project Period (FY) |
1985 – 1987
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| Keywords | Subarachnoid hemorrhage / Cerebrospinal fluid / Endothelium-dependent contraction |
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| Research Abstract |
We have reported the ACh produces endothelium-dependent contractile (EDC) response in canine cerebral artery, and a possible endothelium-derived contracting factor (EDCF) is TXA_2. The present experiments were undertaken to elucidate whether the cerebrospinal fluid (CSF) collected from the patients suffered from subarachinoid hemorrhage (SAH) causes EDC response in canine cerebral artery, and to determine spsmogenic substances in the fulid and explore its antagonist. The sample prepared from the CSF collected from the patients suffered from SAH caused EDC response in canine cerebral artery and the response was inhibited by phospholipase inhibitor, lipooxygenase inhibitor, cyclooxygenase inhibitor, TXA_2 synthetase inhibitor and TXA_2 antagonist. ATP,ADP and AMP, whith are released from hemolysate and platelet,caused EDC response in canine cerebral artery. The EDC response induced by A-23187 was more strongly inhibited by nifedipine than that indeced by TXA_2 analogue, STA_2. The present studies demonstrated that CSF obtained from the patients suffered from SAH stimulates endothelium and releases TXA_2-like substances, requiring Ca_<2+> mobilization. It was quggested that possible substances to stimulate endothelium are adenine nucleotides and the spasm following SAH may be inhibited by TXA_2 synthetase inhibitor and its antagonist, or specific Ca_<2+> antagonists against TXA_2-induced Ca^<2+> mobilization.
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