Journal of Clinical & Experimental Pathology
Open Access

Abstract

Background: Risks of postoperative neurological disorders continue to have a significant impact on quality of life and vital prognosis in cardiac surgical patients. Ischemic postconditioning (IPOC) may be a way to protect against cerebral postoperative complication after cardiac operation. Purpose: The study aimed the investigation of the neuroprotective effect of IPOC in rat with complete global cerebral ischemia- reperfusion injury, which was modeled eversible occlusion of the major vessels originating from the aortic arch. Methods: Complete global cerebral ischemia-reperfusion was induced in male Wistar rats by tr. brachiocephalicus, a. subclavia sin, and a. carotis communis sin. Occlusion-reperfusion. The animals were randomized into one of the following groups: 1) sham; 2) controls: 10-min ischemia/48-h reperfusion; 3) IPOC: 3 cycles of 15-s reperfusion/15-s ischemia were applied just after 10- min ischemia followed by 48-h reperfusion. Neuronal death all fields of the hippocampus was detected by hematoxylin and eosin staining. Bax expression was measured by immunohistochemistry. Lactate dehydrogenase (LDH) activity and creatinine levels in serum were also detected. Results: Hippocampal CA1, СА3 neuronal death was significantly reduced in the IPOC group. It is shown that IPOC in the CA1, CA3 hippocampus also significantly to reduce the number of Bax-positive neurons. LDH activity was found to be significantly increased after 48 h of reperfusion in controls as compared to sham-treated animals, but is not found differences by IPOC group. Conclusions: Cerebral IPOC on models of complete global cerebral ischemia-reperfusion injury in rats can inhibit CA1, CA3 neuronal death. Neuroprotective effect of IPOC is likely achieved by preventing apoptosis of neurons in the most sensitive to ischemic injury of the brain.

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