[Effect of calcium entry blocker, nimodipine, on the cerebral function and metabolic recovery following experimental cerebral ischemia].

Ischemic deporalization of cell membranes is associated with a precipitous influx of calcium from the extracellular to the intracellular compartment, and it is suggested that increased intracellular calcium in ischemic brain leads to an activation of phospholipase and to increase of the concentration of free fatty acids, in particular arachidonic acid, with energy depletion. The objective of the present study is to test whether calcium entry blocker, nimodipine, prevent increase of free fatty acids and metabolic disturbances during ischemic period, and promote functional and metabolic recovery after recirculation. Severe forebrain ischemia in rats was induced by four-vessel occlusion with reducing the systolic arterial pressure to 100 mmHg. After forebrain ischemia had been maintained for 30 minutes, recirculation was started by removal of the arterial clamps of bilateral common carotid arteries and by increasing systemic blood pressure to the preischemic level. The EEG was continuously recorded from gold-coated screws inserted bilaterally in the parietal bones with the tips in extradural position, against a reference inserted prefrontal bone. Analysis of power spectrum of EEG activity was done by Berg Fourier Analyser. The brain were frozen in situ with liquid nitrogen before, during and after ischemia and then chiselled out during irrigation with liquid nitrogen. Concentrations of ATP, ADP, AMP and free fatty acids in brain tissue were determined with high performance liquid chromatography. Nimodipine, 10 micrograms/kg, was given intravenously 2-3 minutes before induction of ischemia, and an infusion of 1 microgram/kg/min was continued during ischemic and postischemic periods.(ABSTRACT TRUNCATED AT 250 WORDS)