Abstract
The aim of the present work was to study the effects of ischemic postconditioning (IPC) on neuron viability in hippocampal field CA1 and cytoplasmic lactate dehydrogenase (LDH) activity in these cells in 30 male Mongolian gerbils (Meriones unguiculatus). Ischemic brain damage was modeled by bilateral occlusion of the common carotid arteries for 7 min. IPC was produced using three episodes of reperfusion-ischemia, 15 sec/15 sec. Morphometric analysis and histoenzymological LDH assay in the cytoplasm of hippocampal field CA1 neurons were performed 48 h after reperfusion, with quantitative cytometric assessment of enzyme activity. The results showed that 7-min ischemia led to a decrease in the number of viable neurons (to 24%) and decreased their LDH activity (from 0.260 ± 0.009 to 0.190 ± 0.006 units). Use of IPC led to a significant increase in the number of viable hippocampal field CA1 neurons (to 52.9%, p < 0.01), which was accompanied by an increase in their LDH activity (to 0.240 ± 0.008 units, p < 0.001).
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