6533b825fe1ef96bd128278a

RESEARCH PRODUCT

Identification and role of inflammatory oxygen free radicals in cardiac ischemia and reperfusion injury

subject

description

Prolonged myocardial ischemia results in a variety of severe cellular, metabolic and ultra-structural damages. It is therefore generally accepted that reperfusion is an absolute prerequisite for the survival of ischemic tissue. However, reperfusion may precipitate arrhythmias, cause myocardial stunning and accelerate necrotic process. Oxygen free radicals have been suggested as possible mediators of reperfusioninduced injury and there is circumstantial evidence that supports this hypothesis. Indirect evidence in support of this concept derives from studies in which antioxidant enzymes, enzyme inhibitors, free radical scavengers and iron chelators are able to protect against reperfusion injury in a number of experimental studies.In vivopolymorphonuclear leukocytes (PMNs) have been hypothesized to induce and to amplify the process of reperfusion injury in post-ischemic myocardium. Within vivo models, there are many different cellular and humoral factors making it difficult to determine the importance of specific components in the pathogenesis of myocardial injury. Both ischemia and reperfusion promote the expression of pro-inflammatory gene products and bioactive agents. Furthermore, ischemia induces a pro-inflammatory state that increases tissue vulnerability towards further injury during reperfusion.