Key result
Post-subarachnoid cerebral vasospasm stems primarily from smooth muscle contraction rather than structural wall changes.
Answers are grounded in this paper and cite their sources.
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.
No takes yet. Share an insight, caveat, or question.
Macdonald et al. (1992) conducted a review in Subarachnoid hemorrhage (SAH). Subarachnoid hemorrhage vs. Normal middle cerebral arteries was evaluated on Mechanism of cerebral vasospasm (arterial wall changes). Cerebral vasospasm following subarachnoid hemorrhage in monkeys appears to be primarily driven by vascular smooth muscle contraction rather than arterial wall hypertrophy, hyperplasia, or fibrosis.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: