The role of vasopressin in acute cerebral vasospasm

Abstract

An experimental model of subarachnoid hemorrhage (SAH) in the Sprague-Dawley rat induces angiographically demonstrable, reproducible biphasic vasospasm of the vertebrobasilar system. The acute vasospasm is maximum at 10 minutes and the maximum late vasospasm occurs 2 days after the SAH. Brattleboro rats, which are deficient in arginine vasopressin (AVP), do not have acute vasospasm after SAH but exhibit a degree of late vasospasm that is not significantly different from that seen in Sprague-Dawley rats. Cisternal injection of AVP induced acute vasospasm in Sprague-Dawley rats with a duration similar to that seen after cisternal blood injection; however, at 2 days, the vessel diameter was normal. Intravenous AVP antagonist or intracisternal AVP antiserum administered prior to the SAH prevented the development of acute vasospasm without affecting the late phase. The data suggest that an increased release of AVP in the cerebrospinal fluid is involved in the development of acute cerebral vasospasm.