| Project/Area Number |
01570804
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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 |
Cerebral neurosurgery
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| Research Institution | Gifu University |
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Principal Investigator |
YAMADA Hiromu Gifu University School of Medicine Neurosurgery Professor, 医学部, 教授 (40021365)
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| Co-Investigator(Kenkyū-buntansha) |
NISHIMURA Yasuaki Gifu University School of Medicine Neurosurgery Assistant Professor, 医学部附属病院, 講師 (60198512)
ANDOH Takashi Gifu University School of Medicine Central Surgical Center Associate Professor, 医学部附属病院, 助教授 (90126722)
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| Project Period (FY) |
1989 – 1991
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| Project Status |
Completed (Fiscal Year 1991)
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| Budget Amount *help |
¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1991: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1990: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1989: ¥500,000 (Direct Cost: ¥500,000)
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| Keywords | Subarachnoid hemorrhage / Cerebral vasospasm / Leukotriene / Oxyhemoglobin / Cystosolic calcium / Phospholipase C / 細胞内カルシウムイオン / イノシト-ルリン脂質特質的ホスホリパ-ゼC / 破裂脳動脈瘤 / アラキドン酸 / 細胞内遊離カルシウム / GTPー結合蛋白質 / イノシト-ルリン脂質特異的ホスホリパ-ゼ / アラキドレ酸 |
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| Research Abstract |
The purpose of this study was to clarify the role and action of leukotriene, arachidonic acid and lipid metabolites in the mechanism of cerebral vasospasm following aneurysmal subarachnoid hemorrhage(SAH). The following results were obtained : (1) In the experimental SAH, vertebral angiogram showed a tripple phase reaction of canine basal arteries caused by the intrathecal injection of leukotriene C_4. (2)In cultured rat vascular smooth-muscle cells, changes in the concentration of cytosolic calcium([Ca^*]i)before and after exposure to spasmogenic factors were measured. Leukotriene C_4 induced a slow, transient increase of[Ca^*]i. Oxyhemoglobin induced a significant elevation of[Ca^*]i which was sustained for 10 minites. (3)In the CSF of SAH patients, there is a marked elevation of the content of membrane lipids, and the activity of phospholipase C was enhanced in proportion to clinical grade according to Hunt and Hess during the early period after SAH. (4)The CSF of SAH patients induced significantly higher transient intracellular calcium elevations when compared to those induced by control CSF. Changes in intracellular free calcium elevations induced by CSF showed a biphasic response with highest concentration on Day 2 and 11 after SAH.
The results suggested that some substances which induce the re-elevation of intracellular calcium concentrations in vascular smooth-muscle cells may be the key substances responsible for cerebral vasospasm.
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