Abstract

The aim of the present work was to investigate the effects of ischemic postconditioning (iPostC) on the viability of neurons in the various hippocampal fields and on cytoplasmic succinate dehydrogenase (SDH) activity in 30 Mongolian gerbils (Meriones unguiculatus). Ischemic brain damage was modeled by bilateral occlusion of both carotid artery for 7 min. iPostC was reproduced using three episodes of reperfusion (15 sec) and ischemia (15 sec). At 48 h after reperfusion, morphometric analysis was performed, along with histoenzymatic assessment of SDH activity in the cytoplasm of pyramidal neurons in hippocampal fields CA1, CA2, CA3, and CA4. The results of these studies showed that 7-min ischemia leads to significant decreases in the proportions of unchanged neurons in hippocampal fields CA1 (to 24%) and CA3 (to 56%); all hippocampal fields showed increases in cytoplasmic SDH activity, as compared with values in sham-operated animals. Use of iPostC led to significant increases in the proportion of unchanged neurons in hippocampal field CA1 (to 52.9%, p < 0.01) and field CA3 (to 88%, p < 0.05), which were accompanied by decreases in SDH activity in surviving neurons in all hippocampal fields.

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