1990 Fiscal Year Final Research Report Summary
Experimental Study of the Mechanism of Cerebral Vasospasm
| Project/Area Number |
01480357
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | Kagawa Medical School |
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Principal Investigator |
OHMOTO Takashi Kagawa Med. Sch., Neurological Surgery, Professor, 医学部, 教授 (60032900)
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| Co-Investigator(Kenkyū-buntansha) |
HONMA Yutaka Kagawa Med. Sch., Neurological Surgery, Research Associate, 医学部, 助手 (60209343)
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| Project Period (FY) |
1989 – 1990
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| Keywords | Subarachnoid Hemorrhage / Cerebral Vasospasm / Changes in Permeability / Bood Arterial Wall Barrier / Trancer Study / Endothelial Injury |
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| Research Abstract |
Adult cats were subjected to this study in order to examine the changes in permeability of major cerebral arteries after subarachnoid hemorrhage by using three kinds of tracers (horse raddish peroxidase, native ferritin, colloidal gold).
In this model, vasospasm was induced in the basilar artery after two injections of autologous blood into the cisterna magna. Tracers were observed in the endothelial plasmalemmal vesicles, interendothelial spaces, subendothelial spaces, and widened intercellular spaces in the smooth muscle layer. Most noticeable routes to the smooth muscle layer appeared to be interendothelial spaces with broken tight junctions following subarachnoid hemorrhage. In the mormal basilar artery, no tracer was observed in the vessel wall.
These results suggest that intraluminal vasoactive substances may penetrate the vessel wall of major cerebral arteries in the early stage of subarachnoid hemorrhage, resulting in the progressive and long-lasting vasospasm. These permiability changes of major cerebral arteries may play an important role in the pathogenesis of cerebral vasospasm.
In experimental endothelial injury was produced by arterial perfusion with low or high osmolar agents. After perfusion, arterial diameter gradually decreased. In these vessels, ultrastructural changes, which were similar to those of spastic arteries after subarachnoid hemorrhage, were seen. Intraarterial injection of tracers revealed the increased permeability of the arterial walls. Biochemical endothelial injury with increased permiability resulting from subarachnoid hemorrhage may thus be importantly involved in the pathogenesis of cerebral vasospasm.
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