title: The role of inflammation in experimental cerebral vasospasm.
abstract: The short-term (less than or equal to 72-hour) cerebral vascular reaction to subarachnoid injectates of various specific blood components was determined by angiography in a canine model of cerebral vasospasm. Cell-free subarachnoid clots of autologous plasma in the basal cistern were found to produce no significant reaction of the basilar artery, while whole-blood clots induced a small (15%) chronic constriction after 24 hours. Because the plasma clots were not well retained in the basal cistern, however, small beads (dextran or latex) were added to stabilize them. Injection of beads and plasma led to moderate-to-severe chronic vasoconstriction (35% to 40%) with rapid onset. Control experiments demonstrated that these foreign bodies (beads) alone induced this vascular reaction. Histological examination showed that severe inflammation followed the introduction of subarachnoid beads. The experiments demonstrate that inflammation alone, in the absence of other processes associated with subarachnoid hemorrhage, may induce persistent and severe cerebroarterial constriction and raises the possibility that inflammation in response to subarachnoid blood may play a role in clinical vasospasm.
authors.affiliation: Laboratory for Cerebrovascular Biophysics, Massachusetts General Hospital, Boston.
authors.forename: J W
authors.initials: JW
authors.lastname: Peterson
authors.forename: B D
authors.initials: BD
authors.lastname: Kwun
authors.forename: J D
authors.initials: JD
authors.lastname: Hackett
authors.forename: N T
authors.initials: NT
authors.lastname: Zervas
mesh_terms: D000818:Animals; D001488:Basilar Artery / Q000000981:diagnostic imaging; D002533:Cerebral Angiography; D004195:Disease Models, Animal; D004285:Dogs; D005549:Foreign-Body Reaction / Q000209:etiology; D007249:Inflammation / Q000503:physiopathology*; D002542:Intracranial Embolism and Thrombosis / Q000473:pathology / Q000503:physiopathology; D002546:Ischemic Attack, Transient / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D013345:Subarachnoid Hemorrhage / Q000473:pathology / Q000503:physiopathology; D013346:Subarachnoid Space / Q000473:pathology