Abstract

MECHANISMS OF CEREBRAL ISCHEMIA-REPERFUSION INJURY: A REVIEW

Dr. R. Padmavathi*

ABSTRACT

Stroke is becoming more common over the world at an alarming rate. In the case of a stroke, reperfusion therapy is thought to be the most life-saving treatment. Reperfusion of the ischemic area, on the other hand, has been found to exacerbate the original damage induced by ischemia. The mechanisms of reperfusion damage have been the subject of extensive research. Reperfusion therapy combined with anti-reperfusion-injury medications has been shown to be more successful in reducing post-stroke complications. Understanding the pathophysiology of reperfusion injury is therefore critical for developing neuroprotectants that increase reperfusion therapy efficacy. An attempt was done to make a review on mechanisms underlying the reperfusion injury. The mechanisms of ischemia-reperfusion injury have been suggested to include oxidative stress, leukocyte infiltration, platelet adhesion and aggregation, complement activation, mitochondrial mediated mechanisms, and blood-brain-barrier (BBB) disruption, which all lead to edoema or hemorrhagic transformation (HT) in the brain, according to growing experimental evidence. Apoptosis, autophagy, necrosis, and necroptosis are all possible outcomes of prolonged ischemia-reperfusion injury. The latest mechanistic insights into reperfusion-injury-induced cell death via these several mechanisms are highlighted. The interconnected signalling pathways of cell death could provide novel therapeutic targets. Ischemia-reperfusion damage treatment options are also discussed. We believe that gaining a better understanding of the process of ischemia-reperfusion injury will lead to the development of new treatment options.

Keywords: Reperfusion injury; Reactive oxygen metabolites; Polymorphonuclear leukocytes.