Morphofunctional Characteristics of the Microcirculatory Bed and Neurons in the Neocortex after Ischemic Postconditioning

Abstract

Expression of PECAM-1/CD31 protein (a biomarker for endothelial function and neovascularization processes) was studied in microvessels in layers II, III, and V of the cerebral cortex in Mongolian gerbils (Meriones unguiculatus) in the early (day 2) and late (day 7) parts of the reperfusion period after 7-min forebrain ischemia, ischemic postconditioning (iPostC), and sham-operated animals (n = 60). In the latter, the lowest level of PECAM-1/CD31 immunoreactivity was seen in structures in layer III of the cerebral cortex. Reversible ischemic brain injury decreased the number of morphologically unaltered neurons in the neocortex with increases in the duration of the reperfusion period; cortical layers II, III, and V also showed increased levels of PECAM-1/CD31 immunoreactivity with significant increases in the late reperfusion period. iPostC consisting of three stimulatory episodes of reperfusion-ischemia (15/15 sec) led to significant increases in the number of morphologically unaltered neurons and PECAM-1/CD31 immunoreactivity in layers II and III in the early reperfusion period. In the later reperfusion period following iPostC, the number of unaltered neurons in layers II, III, and V of the cortex increased, while the level of PECAM-1/CD31 immunoreactivity decreased significantly. The results lead to the conclusion that the cytoprotective effect of iPostC in forebrain ischemia is mediated by a physiological adaptive mechanism leading to increases in PECAM-1/CD31 immunoreactivity in cortical microvessels in the early reperfusion period and a decrease in the later reperfusion period.