The potent, centrally active, calcium channel antagonist, nimodipine, was utilized in a highly predictive "spinal stroke" model in order to investigate the potential pathophysiological effects of calcium flux in spinal injury, as well as to evaluate the potential therapeutic role of the newly developed dihydropyridine derivatives in ischemic central nervous system injury. Nimodipine, administered before or after ischemia, at doses shown to be effective in improving cerebral blood flow and in dilating central blood vessels, failed to improve either the histopathological changes or the functional deficit caused by temporary aortic occlusion in the unanesthetized rabbit.
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Faden et al. (1984) studied this question.
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