Pathogenesis of cerebral vasospasm.
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 play a major role in the propagation of the process, it is possible that therapy directed at preventing platelet accumulation may interrupt the cycle.
D000818:Animals; D002536:Cerebral Arteries / Q000473:pathology; D004727:Endothelium / Q000473:pathology; D002532:Intracranial Aneurysm / Q000473:pathology; D002546:Ischemic Attack, Transient / Q000473:pathology*; D008251:Macaca; D008854:Microscopy, Electron; D009131:Muscle, Smooth, Vascular / Q000473:pathology; D010973:Platelet Adhesiveness; D012422:Rupture, Spontaneous; D013345:Subarachnoid Hemorrhage / Q000473:pathology