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Cerebral arteries from monkeys with chronic cerebral vasospasm arising from experimental subarachnoid hemorrhage produced 5-6 days previously were examined for changes in their functional properties in an attempt to understand the basis of the narrowing. Hemorrhage was caused by puncture of the internal carotid artery just proximal to the circle of Willis. Segments taken close to the origins of the anterior and middle cerebral arteries consistently showed decreased distensibility. In addition, they exhibited large, prolonged, spontaneous increases in muscle tone. Other alterations observed include a marked reduction in the capacity of the vessel wall to contract, reduction in constrictor and dilator nerve influences on vascular tone, and some increased sensitivity to serotonin. Small pial arteries (150-200 micron o.d.) from the side of the injury showed large spontaneous irregular increases in tone. It is proposed that 5-6 days after experimental subarachnoid hemorrhage in monkeys the change most responsible for persistent narrowing in the larger arteries is an increased rigidity of the vessel wall. This is probably caused by an inflammatory response. In the smaller arteries, abnormal spontaneous contractile activity is a major factor in narrowing. This activity is not stretch-dependent. We suggest that the initial cause of the arterial narrowing after hemorrhage is the action of vasoactive substances released in the close vicinity of the arterial wall, which lead to tissue damage, abnormal tone, and an inflammatory response with fibrosis.

Functional arterial changes in chronic cerebrovasospasm in monkeys: an in vitro assessment of the contribution to arterial narrowing.