to study progression of apoptosis and alterations in brain ADP-ribosyl cyclase activity during early postischemic period. Material & Methods: modeling of acute ischemic damage of brain was performed with a method of right carotid artery clamping in rats of experimental (duration of postischemic period was 24 and 48 hr) and control groups (n=25). In thin brain slices, apoptosis has been detected with TUNEL method. Activity of ADP-ribosyl cyclase has been measured fluorimetrically in brain tissue homogenates. Results: We found significant increase of the enzyme activity in neurons of frontal and occipital regions of brain in a zone of ischemia during 24 hr of early postischemic period followed by the activity's fall at 48 hr. Also, inhibition of ADP-ribosyl cyclase activity in intact hemisphere was revealed at 48 hr after ischemia. We were able to detect changes in apoptosis progression in various brain regions throughout the postischemic period. Conclusions: Pathogenetic role of alterations of ADP-ribosyl cyclase activity in initiation and progression of neuronal apoptosis induced by ischemia is postulated.
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