[Postischemic reperfusion and "reperfusion paradox" in ischemic stroke]

Current therapeutic approaches for the acute phase of ischemic stroke (IS) primarily involve advanced reperfusion technologies aimed at restoring blood flow to areas with reduced perfusion. However, even with successful restoration of blood flow through the affected vessel, reperfusion injury can intensify tissue damage by exacerbating metabolic disorders and triggering programmed cell death in the ischemic region. Consequently, the effectiveness of treatment and overall outcomes are heavily influenced by the extent of reperfusion injury. This review presents the latest insights into the key stages of the ischemic-hypoxic cascade and the ischemia/reperfusion associated with IS. It discusses the characteristics of the molecular and cellular responses to postischemic reperfusion, identifies the primary factors contributing to reperfusion injury, and explores various manifestations of the «reperfusion paradox». Furthermore, the review addresses therapeutic strategies aimed at mitigating the adverse effects of hypoxia-induced damage.