We report the regional variation in [3H]nimodipine binding in vivo during focal cerebral isch emia. After intravenous injection, 30 min of circulation of eH]nimodipine was sufficient to establish a secular equi librium of distribution in the brain. Rats sustained left middle cerebral and common carotid artery occlusions for 5 min, and 4, 24, and 48 h (n ?o 6 per group). They were decapitated 30 min after injection of 250 /l-Ci of eH]nimodipine and their brains were submitted to auto

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... The concentrations of r3Hjnimodipine in plasma and brain structures, corrected for metabolism of nimodipine, were used to calculate the regional volumes of distribution (V) in the ischemic left (L) and control right (R) hemispheres. Log (VdVR) was then defined as the group mean of the logarithms of the left-to-right ratio of V of eH]nimodipine. In the lateral caudate, binding of eH]nimodipine on the ischemic side was highest within 5 min of occlusion. Log (V dV R) in this region for the com bined sham-operated and normal control rats and those after 5 min and 4 and 24 h of ischemia were -0.014 ± Interruption of cerebral blood flow initiates the suppression of neuronal activity by anoxia. A vari ety of biochemical and membrane-related events are unleashed by the decline in blood flow and ar rest neuronal activity. However, ischemic tissue is not inevitably committed to infarction. Border-zone ischemia (