{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,10]],"date-time":"2025-09-10T22:50:21Z","timestamp":1757544621535},"reference-count":21,"publisher":"Journal of Neurosurgery Publishing Group (JNSPG)","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[1977,3]]},"abstract":"<jats:p content-type=\"fine-print\">\u2713 In anesthetized dogs, subarachnoid hemorrhage (SAH) was induced by the mechanical rupture of the unilateral intracranial internal carotid artery. Vasospasm was angiographically determined 24 hours and 7 days after SAH. Contractile responses to serotonin, norepinephrine, histamine, and K<jats:sup>+<\/jats:sup> were compared in control and bleeding sides of the middle cerebral arteries removed from dogs with SAH, and from sham-operated dogs. Under sham operation and 2 hours after SAH, responses in the arteries of both sides did not appreciably differ but response was significantly less in arteries from the bleeding side as compared with the control side 24 hours and 7 days after hemorrhage. However, median effective concentrations of serotonin, histamine, and K<jats:sup>+<\/jats:sup> were approximately the same in the arteries from both sides. Vasospasm and decreased sensitivity to the vasoactive agents of middle cerebral arteries were reversed 42 days after SAH. It is thus quite likely that initiation and maintenance of post-hemorrhage vasospasm is not associated with an increase in the sensitivity of cerebral arteries to vasoconstricting endogenous substances, rather the state of decreased sensitivity of cerebral arteries in contact with SAH may be instrumental in relieving prolonged vasospasm.<\/jats:p>","DOI":"10.3171\/jns.1977.46.3.0296","type":"journal-article","created":{"date-parts":[[2009,5,7]],"date-time":"2009-05-07T15:20:46Z","timestamp":1241709646000},"page":"296-303","source":"Crossref","is-referenced-by-count":44,"title":["Cerebrovascular sensitivity to vasoconstricting agents induced by subarachnoid hemorrhage and vasospasm in dogs"],"prefix":"10.3171","volume":"46","author":[{"given":"Noboru","family":"Toda","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Takashi","family":"Ozaki","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tomio","family":"Ohta","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1754","reference":[{"key":"b1","series-title":"J Neurosurg","doi-asserted-by":"publisher","first-page":"440","DOI":"10.3171\/jns.1974.41.4.0440","article-title":"Experimental catecholamine-induced chronic cerebral vasospasm. 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