Postconditioning – a mechanism for prevention of ischemia/reperfusion injury

Abstract

Introduction. Ischemia is a pathological condition when the blood supply to a tissue is interrupted and may lead to irreversible damages due to lack of oxygen and nutrients. There are many diseases, such as myocardial infarction, ovarian torsion, ischemic stroke, where the quick intervention of the physician may save the organ from necrosis. The first treatment option is to remove the cause of ischemia, but the studies revealed that the reperfusion is able to worsen the initial lesions that were only due to disrupted blood flow. The scientists propose postconditioning as a technique for reducing the reperfusion injuries.Aim of the study. The aim of the study was to do a research of the specialized literature to assure a better understanding of the mechanisms of protection of postconditioning in the context of the diseases characterized by ischemia/reperfusion injuries. Materials and methods. Were studied the articles from PubMed database over the last ten years describing the mechanisms of ischemia/reperfusion injury in different organs and the effects of postconditioning as a method of protection against reperfusion lesions. Were used the following keywords: postconditioning, ischemia/reperfusion injury. Results. The reperfusion injuries are due to activation of different metabolic pathways that are related to toxic compounds formation, such as reactive oxygen species (ROS), with deleterious effects on cell components. The studies revealed that during reperfusion the level of malonic dialdehyde, a biomarker for membrane lipid peroxidation, increases, and this is due to a high level of ROS. Moreover, the literature related to reperfusion injury emphasizes the role of the increased intracellular calcium concentration with activation of different enzymes, the opening of the mitochondrial permeability transition pore, inflammation, increased endothelial dysfunction, and neutrophils activation. Postconditioning after ischemia involves short-term cycles of ischemia that alternate with reperfusion, at the onset of the restoration of the blood flow. It was established that the mechanisms of protection are considered to be related to a reduction of ROS production, inhibition of mitochondrial permeability transition pore, activation of ATP-dependent K-channel through adenosine, which affects the intracellular calcium levels, nitric oxide and pro-survival kinase. Conclusions. Postconditioning which represents the gradual restoration of blood flow can reduce the extent of reperfusion injury by various mechanisms. The results of the experimental studies on different ischemic organs showed that the short episodes of interruption of the blood flow from the onset of reperfusion, essentially reduced the size of the lesion, compared to a normal revascularization. The postconditioning must be taken into account when there are ischemic diseases.