NA;The effect of nimodipine on the in vitro reactivity of cerebral vessels after subarachnoid hemorrhage lpar;SAHrpar; was studied. With the use of a primate model of chronic cerebral vasospasm, 12 female cynomolgous monkeys underwent the induction of a SAH by the direct placement of an average 6.4hyphen;ml autologous hematoma against the major anterior cerebral vessels in the right basal subarachnoid spaces lpar;Day 0rpar;. The animals were then randomized to one of four groups and within 14 to 20 hours after clot placement were started on oral q8h therapy with nimodipine lpar;3, 6, or 12 mgsol;kgrpar; or placebo. On Day 7, the animals were killed and the right and left middle cerebral arteries lpar;MCAsrpar; were immediately resected and placed in oxygenated Krebs' solution. Ring preparations from the arteries were suspended in organ baths, and dosehyphen;effect curves to varying concentrations of norepinephrine, 5hyphen;hydroxytryptamine, and potassium chloride were obtained. There was a highly significant reduction in the response of the MCA on the clot side lpar;rightrpar; relative to the nonclot side lpar;leftrpar; to all three agonists. The clot side contractility was not influenced by nimodipine treatment at any of the four doses tested. The nonclot side arteries of the 12hyphen;mgsol;kg treatment group demonstrated significantly enhanced reactivity for all three agonists. Oral treatment with high dose nimodipine enhances the reactivity of normal cerebral vessels to the agonists tested, but it does not seem to affect the reactivity of arteries in chronic spasm at any of the four doses tested. lpar;Neurosurgery16colon;137hyphen;140, 1985rpar;
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