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Mechanism of Cerebral Vasospasm Following Subarachnoid Hemorrhage in Monkeys

Published online by Cambridge University Press:  18 September 2015

R.L. Macdonald*
Affiliation:
Division of Neurosurgery, University of Alberta, Edmonton
B.K.A. Weir
Affiliation:
Division of Neurosurgery, University of Alberta, Edmonton
M.G.A. Grace
Affiliation:
Department of Surgery, University of Alberta, Edmonton
M.H. Chen
Affiliation:
Medicine-Dentistry Electron Microscopy Unit, University of Alberta, Edmonton
T.P. Martin
Affiliation:
Faculty of Medicine, and Faculty of Rehabilitation Medicine, University of Alberta, Edmonton
J.D. Young
Affiliation:
Department of Physiology, University of Alberta, Edmonton
*
60 Fairleigh Crescent, Toronto, Ontario, Canada M6C 3R9
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Abstract:

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This paper reviews our recent studies on the mechanism of cerebral vasospasm following subarachnoid hemorrhage (SAH) in monkeys. Middle cerebral artery (MCA) vasospasm was maximal at 7 days, resolving by 14 days, and absent at 28 days after SAH. Arterial fibrosis was not detected during vasospasm, although there was intimal hyperplasia with fibrosis 28 days after SAH. On scanning electron microscopy, smooth muscle cells from vasospastic arteries had corrugated cell membranes and appeared similar to cells contracted pharmacologically, suggesting that vasospastic smooth muscle is contracted. Morphometric analysis of arteries obtained 7 days after SAH showed no significant increases in arterial wall area of vasospastic arteries compared with normal MCAs. The results suggest vasospasm in monkeys is not due to hypertrophy, hyperplasia, or fibrosis in the arterial wall. Vasospasm may be mainly vascular smooth muscle contraction, which damages the arterial wall, leading to secondary structural changes in the arterial wall which occur after angiographic vasospasm.

Type
Articles
Copyright
Copyright © Canadian Neurological Sciences Federation 1992

References

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