{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T20:54:50Z","timestamp":1788382490952,"version":"build-2803163510"},"reference-count":43,"publisher":"Journal of Neurosurgery Publishing Group (JNSPG)","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[1995,9]]},"abstract":"<jats:p content-type=\"fine-print\">\u2713 To investigate the effects of subarachnoid hemorrhage (SAH) on the responsiveness of human cerebral arteries to vasoactive substances, the authors measured the isometric tension generated in helical strips of basilar and middle cerebral arteries isolated from human cadavers Contractions caused by KCl, prostaglandin F<jats:sub>2\u03b1<\/jats:sub>, noradrenaline, and serotonin were reduced in arteries obtained from cadavers with aneurysmal SAH damage and compared to those obtained from cadavers with no indication of intracranial diseases. Endothelium-dependent relaxation elicited by substance P and bradykinin, and endothelium-independent relaxation induced by prostaglandin I<jats:sub>2<\/jats:sub>and nitroglycerin were also markedly decreased in arteries affected by SAH. However, the reduction in relaxation response to prostaglandin I<jats:sub>2<\/jats:sub>was significantly less than that to the other vasodilator agents. These results indicate that human cerebral artery functions are severely impaired after SAH and that poor responses to vasoactive agents may result primarily from dysfunction of smooth-muscle cells.<\/jats:p>","DOI":"10.3171\/jns.1995.83.3.0510","type":"journal-article","created":{"date-parts":[[2009,6,2]],"date-time":"2009-06-02T17:58:10Z","timestamp":1243965490000},"page":"510-515","source":"Crossref","is-referenced-by-count":42,"title":["Altered reactivity of human cerebral arteries after subarachnoid 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