[Experimental studies on pharmacologic protection of the brain against focal ischemia.  2.  Effects of KB-2796 and nicardipine on focal brain ischemia in rats]. 
It has been proposed that calcium overload triggers neuronal cell damage in the acute stage of cerebral ischemia.  In this study, the effects of calcium antagonists, KB-2796 and nicardipine, on neurologic deficits and size of the infarction were studied in the rat middle cerebral artery (MCA) occlusion model.  Neurologic deficits were evaluated from 1 to 24 hours after occlusion of the MCA, using a grading system of Bederson et al.  At 24 hours post-occlusion, the brain was removed, sliced coronally, and stained with triphenyltetrazolium chloride.  Size of the infarction was measured by computerized image analysis system.  KB-2796 (10 mg/kg) or nicardipine (1 mg/kg) was intraperitoneally administered immediately after occlusion of the MCA.  In the KB-2796-treated group, the neurologic deficits were much improved and the size of infarction was significantly smaller, but in the nicardipine-treated group improvement was modest and did not reach the level of statistical significance.  The neurologic improvement was observed in the group where KB-2796 was given at 3 hours post-occlusion but the size of infarction was unchanged.  The results in the present study seem to indicate that the calcium antagonists could improve focal cerebral ischemia when administered in early stage of ischemia, and that such effect is more significant with KB-2796 probably because of its higher selectivity to the cerebral vessels.