[Postconditioning is a universal protective phenomenon].
The analysis of the data available in the literature shows that postconditioning enhances cardiac tolerance to the arrhythmogenic impact of reperfusion, prevents the occurrence of the no-reflow phenomenon, and eliminates cardiomyocytic necrosis and apoptosis during reperfusion. Independent clinical observations indicate the high clinical efficiency of postconditioning in patients with acute myocardial infarction. The literature data show that postconditioning enhances the tolerance of the brain, spinal cord, kidneys, liver, intestine, and skeletal muscles to reperfusion injury. The molecular mechanism of the protective action of postconditioning is discussed.
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D000818:Animals; D004285:Dogs; D006801:Humans; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000098:blood supply / Q000503:physiopathology; D007668:Kidney / Q000098:blood supply / Q000378:metabolism / Q000503:physiopathology; D008099:Liver / Q000098:blood supply / Q000378:metabolism / Q000503:physiopathology; D018482:Muscle, Skeletal / Q000098:blood supply / Q000378:metabolism / Q000503:physiopathology; D009203:Myocardial Infarction / Q000378:metabolism* / Q000503:physiopathology / Q000628:therapy*; D015427:Reperfusion Injury / Q000378:metabolism* / Q000503:physiopathology / Q000628:therapy*; D013116:Spinal Cord / Q000098:blood supply / Q000378:metabolism / Q000503:physiopathology