NA;The efficacy of the calcium channel blocker nimodipine in the prevention of chronic cerebral vasospasm lpar;VSPrpar; and delayed ischemia after subarachnoid hemorrhage lpar;SAHrpar; in monkeys was examined in a blind, randomized, placebocontrolled trial. The primate model developed in this laboratory reliably induces chronic cerebral vasospasm and can induce pathologically proven delayed ischemic neurological deficits lpar;DINDsrpar;. With standard microsurgical procedures, an average 6.4hyphen;ml autologous hematoma was placed directly against the major anterior cerebral vessels in the right basal subarachnoid spaces of 24 monkeys. The monkeys were randomized to one of four groups and were treated orally q8h for 7 days with nimodipine lpar;3, 6, or 12mgsol;kgrpar; or placebo. An additional 2 monkeys underwent the surgical procedure without clot placement. Drug administration began between 14 and 20 hours after clot placement. Indices monitored before and after SAH included neurological status, angiographic cerebral vessel caliber, and cerebral blood flow. Significant VSP lpar;25 to 100percnt; reduction in vessel caliberrpar; was present on Day 7 on the clot side in 83percnt; of the animals lpar;P le; 0.001rpar;. There was no significant difference lpar;P 0.05rpar; in the incidence of VSP among the four groups. Similarly, there was no significant difference lpar;P 0.05rpar; in the mean vessel caliber reduction after SAH among the four treatment groups. There was no VSP present on Day 7 in the shamhyphen;operated animals. One animal receiving high dose nimodipine lpar;12 mgsol;kg p.o. q8hrpar; developed a DIND on Day 5 after SAH. A second animal in the 12hyphen;mgsol;kg group developed a transient neurological deficit between Days 4 and 7. lpar;Neurosurgery16colon;129hyphen;136, 1985rpar;
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