Abstract
Visceral infarctions remain the leading cause of mortality in the world, in spite of the development of early reperfusion strategies. Infarct size is determined not only by the severity of ischemia but also by pathological processes initiated at reperfusion. Experimental evidences suggest that brief ischemia-reperfusion periods, called ischemic preconditioning or postconditioning, and performed either before or just after a sustained ischemia, respectively, limit reperfusion injuries. Ischemic conditioning activates several primary pathways that inhibit mitochondrial permeability transition pore opening. Thus, pharmacological interventions like cyclosporine A, a potent permeability transition pore inhibitor, are also able to reduce cell death, when administered at reperfusion (pharmacological postconditioning), in numerous ischemiareperfusion models including in humans. This review will focus on the physiological preclinical data on both ischemic and pharmacological conditioning that are relevant to their translation to clinical therapeutics in intensive care medicine.
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