{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T02:47:10Z","timestamp":1791082030206,"version":"4.1.0"},"reference-count":19,"publisher":"Journal of Neurosurgery Publishing Group (JNSPG)","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[1990,5]]},"abstract":"<jats:p content-type=\"fine-print\">\u2713 The short-term (\u2264 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.<\/jats:p>","DOI":"10.3171\/jns.1990.72.5.0767","type":"journal-article","created":{"date-parts":[[2009,5,13]],"date-time":"2009-05-13T18:20:57Z","timestamp":1242238857000},"page":"767-774","source":"Crossref","is-referenced-by-count":125,"title":["The role of inflammation in experimental cerebral vasospasm"],"prefix":"10.3171","volume":"72","author":[{"given":"John W.","family":"Peterson","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Byung-Duk","family":"Kwun","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John D.","family":"Hackett","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicholas T.","family":"Zervas","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1754","reference":[{"key":"b1","series-title":"J Neurosurg","doi-asserted-by":"publisher","first-page":"923","DOI":"10.3171\/jns.1984.60.5.0923","article-title":"Response of chronic experimental cerebral vasospasm to methylprednisolone and dexamethasone.","volume":"60","author":"Chyatte","year":"1984"},{"key":"b2","series-title":"Stroke","doi-asserted-by":"publisher","first-page":"68","DOI":"10.1161\/01.STR.19.1.68","article-title":"Erythrocytes are essential for the development of cerebral vasculopathy resulting from subarachnoid hemorrhage in cats.","volume":"19","author":"Duff","year":"1988"},{"key":"b3","series-title":"Cerebral Arterial Spasm.","first-page":"139","article-title":"Morphology of the subarachnoid space after subarachnoid hemorrhage","author":"Dujovny","year":"1980"},{"key":"b4","series-title":"Surg Neurol","first-page":"354","article-title":"Cerebral vasospasm.","volume":"5","author":"Heros","year":"1976"},{"key":"b5","series-title":"Ann Neurol","doi-asserted-by":"publisher","first-page":"599","DOI":"10.1002\/ana.410140602","article-title":"Cerebral vasospasm after subarachnoid hemorrhage: an update.","volume":"14","author":"Heros","year":"1983"},{"key":"b6","series-title":"J Neurosurg","doi-asserted-by":"publisher","first-page":"515","DOI":"10.3171\/jns.1978.48.4.0515","article-title":"Cerebral artery spasm. 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