Pathogenesis of cerebral vasospasm in hypertensive encephalopathy

Abstract

A marked increase in cerebrovascular pressure produced mechanically by clamping the aorta resulted in the constriction of small cerebral arteries ranging from 35 to 1000 [mu] in diameter. In addition to this a decreased cerebral blood flow, increased intra-cranial pressure and some perivascular hemorrhages occurred. When the systolic blood pressure becomes greater than 180 mm, cerebral arterial constriction begins and brain swelling occurs. In prolonged instances this results in cerebrovascular compression, brain herniation and compression of the vasomotor center. Brain herniation may produce death unless pressure is reduced. Hypertensive vasospasm is not only due to mechanically produced cerebrovascular hypertension but an agent such as a hypertensive must be used. It irritates the cerebral arterial smooth muscle producing pial arterial constriction decreased pial blood flow and hypoxia.