{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,5]],"date-time":"2025-10-05T16:50:46Z","timestamp":1759683046092},"reference-count":39,"publisher":"Journal of Neurosurgery Publishing Group (JNSPG)","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[1987,6]]},"abstract":"\u2713 The effect of subarachnoid hemorrhage (SAH) on endothelium-dependent vasodilation of the isolated rabbit basilar artery was examined using an isometric tension recording method. The SAH was induced by injecting 5 ml of fresh arterial blood into the cisterna magna. Sixty-two rabbits were separated into four groups according to the timing of sacrifice: control rabbits, and operated rabbits sacrificed on Days 2, 4, and 6 after SAH. Acetylcholine (ACh) (10\u22127<\/jats:sup> M to 10\u22124<\/jats:sup> M) and adenosine triphosphate (ATP) (10\u22127<\/jats:sup> M to 10\u22124<\/jats:sup> M) were used to evoke dose-dependent vasodilation of isolated arterial rings previously contracted by 10\u22126<\/jats:sup> M serotonin (5-HT). There were no significant differences in the vasodilatory response to ACh among these four groups. Relaxation to approximately 84% of the initial contractile tone occurred with 10\u22124<\/jats:sup> M ACh. On the other hand, the vasodilatory response to ATP was suppressed in the animals sacrificed 2 days after SAH; the relaxation of this group was approximately 52% at 10\u22124<\/jats:sup> M ATP, compared to a relaxation of 87% observed in the other groups of animals. One of the major causes of the impairment of endothelium-dependent vasodilation seems to be an inhibition of the production of endothelium-derived relaxing factor by endothelial cells.<\/jats:p>\nAfter the relaxation studies, the dose-response curves for 5-HT were obtained. Serotonin caused significantly more contraction in the animals sacrificed 2 days after SAH than in the other groups. The present experiments suggest that impairment of the endothelium-dependent vasodilation following SAH, together with the potentiation of the contractile response to vasoactive agents in cerebral arteries, may play an important role in the pathogenesis of vasospasm.<\/jats:p>","DOI":"10.3171\/jns.1987.66.6.0915","type":"journal-article","created":{"date-parts":[[2009,5,8]],"date-time":"2009-05-08T16:20:23Z","timestamp":1241799623000},"page":"915-923","source":"Crossref","is-referenced-by-count":66,"title":["Effect of subarachnoid hemorrhage on endothelium-dependent vasodilation"],"prefix":"10.3171","volume":"66","author":[{"given":"Tadayoshi","family":"Nakagomi","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Neal F.","family":"Kassell","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tomio","family":"Sasaki","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shigeru","family":"Fujiwara","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"R. 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