Cerebral arteries have been shown to react to experimental subarachnoid hemorrhage with a nonspecific arterial injury reaction characterized by endothelial cell desquamation, adherence of platelets to the exposed collagen, subendothelial edema, and medial necrosis. This injury reaction is followed by a reparative process with intimal proliferation and medial fibrosis. We have postulated that the arterial narrowing seen by angiography in patients after subarachnoid hemorrhage may be a manifestation of this injury reaction. Because it is likely that the platelets adherent to the damaged endothelium playa major role in the propagation of the process, it is possible that therapy directed at preventing platelet accumulation may interrupt the cycle.