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© 2014, AICH - Servier Research Group. Ischemia and reperfusion of the heart and brain are the leading causes of morbidity and mortality. Conditioning refers to recruiting endogenous protective mechanisms that limit ischemia-reperfusion injury, and is achieved by a number of stimuli administered before, during, or immediately after ischemia and/or reperfusion. Remote ischemic conditioning (RIC) is obtained when brief episodes of ischemia and reperfusion, in one tissue, induce protection in remote tissues. RIC is easily attained by brief inflation/deflation of a blood pressure cuff, or a limb tourniquet, and it provides potent protection against ischemia-reperfusion injury in animal and human models. In clinical studies involving percutaneous coronary interventions, adult and pediatric cardiac surgery, vascular surgery, stroke, and renal transplantation, RIC attenuates end-organ damage. The pathway by which RIC induces protection involves chemical, mechanical, and electrical pathways in the trigger organ. Transfer of the protective signal to the remote organs occurs through neuronal, humoral, and circulating cellular pathways. Our knowledge of the modes and mechanisms of RIC remains incomplete, and a better understanding will help optimize the benefits that can be achieved from this protective reflex. Nonetheless, RIC has achieved early translation into many clinical proof-of-concept trials, and the results of the large outcome studies are eagerly anticipated.


Journal article


Dialogues in Cardiovascular Medicine

Publication Date





241 - 253