{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,23]],"date-time":"2025-09-23T13:16:17Z","timestamp":1758633377312,"version":"3.37.0"},"reference-count":39,"publisher":"Journal of Neurosurgery Publishing Group (JNSPG)","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[1996,3]]},"abstract":"<jats:p content-type=\"fine-print\">\u2713 The purpose of this study was to investigate the effectiveness of oral treatment with the endothelin (ET)<jats:sub>A\/B<\/jats:sub>receptor antagonist Ro 47-0203, 4-<jats:italic>tert<\/jats:italic>-butyl-<jats:italic>N<\/jats:italic>-[6-(hydroxy-ethoxy)-5-(2-methoxy-phenoxy)-2\u2032-bipyrimidin-4-yl]-benzenesulfonamide (bosentan), and the ET<jats:sub>A<\/jats:sub>receptor antagonist 2-benzo[1,3]dioxol-5-yl-3-benzyl-4-(4-methoxy-phenyl)-4-oxobut-2-enoic acid monosodium salt (PD155080), in the prevention of subarachnoid hemorrhage (SAH)\u2014induced delayed cerebral vasospasm. Double hemorrhage in the rabbit constricted the basilar artery to 34% of control as determined by angiography. Oral bosentan and PD155080 administration after the initial SAH decreased the magnitude of constriction to 9% and 16% of control, respectively. Plasma and cerebrospinal fluid bosentan levels and plasma PD155080 levels were consistent with concentrations reported to inhibit ET-1 constriction of blood vessels<jats:italic>in vitro<\/jats:italic>. 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