The efficacy of intravenous nimodipine in the treatment of focal cerebral ischemia in a primate model.

The clinical and pathological effects of nimodipine on cerebral infarction were investigated in 12 male baboons. In randomized/blind trials, six animals given intravenous nimodipine (2 micrograms/kg/min load, 1 microgram/kg/min maintenance) for 96 hours starting 50 minutes before 6-hour double-clip occlusion of the middle cerebral artery were compared to 6 control animals. Standardized neurological examinations were performed by examiners blinded to the animals' therapy on Day 7 and Day 14 after stroke. On Day 14 the animals were killed. The brains were studied pathologically, and the relative areas of infarction were quantified. Intracranial pressure was lower in nimodipine-treated animals; however, the range of intracranial pressure values in each group was broad. Two control animals with high intracranial pressure died. There were no deaths among the nimodipine-treated animals. The neurological scores on Days 7 (P less than or equal to 0.01) and 14 (P less than or equal to 0.05) were significantly different between the two groups. The nimodipine-treated animals had less clinical evidence of infarction compared to controls. Nimodipine-treated animals tended to have smaller areas of infarction; however, the difference between the two groups was not statistically significant. The infusion of nimodipine in the treatment of focal cerebral ischemia is safe and does not appear to aggravate the extent of infarction or to exacerbate intracranial hypertension. The clinical neurological evaluations indicate that nimodipine may improve or preserve neurological outcome after stroke.