1999 Fiscal Year Final Research Report Summary
Role of Early and Excessive Calcium Influx in the Pathogenesis of Cerebral Vasospasm
| Project/Area Number |
10671306
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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 |
SAKAKI Saburo School of Medicine, Ehime University, Professor, 医学部, 教授 (30116933)
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| Co-Investigator(Kenkyū-buntansha) |
OHTA Shinsuke Ehime University Hospital, Assistant Professor, 医学部・附属病院, 講師 (50194163)
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| Project Period (FY) |
1998 – 1999
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| Keywords | calcium / cspase-3(CPP32) / cerebral vasospasm / SAH |
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| Research Abstract |
We have reported that excessive calcium influx into arterial smooth muscle cells occurred in the early phase after experimental subarachnoid hemorrhage (SAH). The role of this overloading of calcium to the arterial smooth muscle cells was studied in the pathogenesis of their degeneration of smooth muscle cells in the spastic artery. Calcium histochemistry showed that intrathecal administration of nicardipine prior to SAH was able to prevent completely excessive calcium influx into the smooth muscle cells after SAH. In the smooth muscle cell layers of spastic arteries, TUNEL positive cells were observed at 7 days after the initial SAH. Intrathecal administration of nicardipine prior to SAH induction was able to reduce the appearance of TUNEL positive cells. In spastic arteries, the time dependent activation of CPP32, which is a protease mediating cell death, was observed at 4 and 7 days after the initial SAH. Inhibition of excessive calcium influx led to a suppression of the activation of CPP32. These results may suggest that excessive calcium influx into the vascular smooth muscle cells activate CPP32 and it plays an important role in the pathogenesis of delayed cerebral vasospasm.
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Research Products
(5 results)
