2001 Fiscal Year Final Research Report Summary
Why is the smooth muscle cell contracted with degeneration in cerebral vasospasm?
| Project/Area Number |
12671364
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | Ehime University |
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Principal Investigator |
OHTA Shinsuke University Hospital, Ehime University, Assistant Professor, 医学部・附属病院, 講師 (50194163)
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| Project Period (FY) |
2000 – 2001
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| Keywords | Cerebral vasopasam / Subarachnoid hemorrhage / Caspase-3 / Calpain / Calcium |
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| Research Abstract |
We elucidated the mechanism of smooth muscle cell degeneration in the basilar arteries with vasospasm by comparing the single- and the double-subarachnoid hemorrhage (SAH) models in which no-arid massive TUNEL positive smooth muscle cells were developed, respectively. Electron microhistochemical study showed that Ca^<++> overloading to the mitochondria was sustained longer after the second SAH induction than the first one in the double-SAH model. Immunohistochemical study showed that while cytochrome c was not detected in the cytosol in the single-SAH model, cytochrome c was released to the cytosol from mitochondria in the smooth muscle cells from 4 to 7 days after the initial SAH in the double-SAH model. Though μ-calpain was transiently activated just after SAH induction in the basilar arteries of the single-SAH model, μ-calpain and caspase-3 (CPP32) was significantly and continuously activated after 4 days in the double-SAH model. In addition, although both amount of Bcl-xl and Bcl-xs which promotes and protects the release of cytochrome c, respectively, was decreased in the basilar arteries 7 days after SAH in the rat SAH model, the ratio between Bcl-xs and Bcl-xl was significantly reduced. These results suggested that the mitochondria dependent sublethal signal may play a significant role in the pathogenesis of the delayed cerebral vasospasm.
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