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Postconditioning and protection from reperfusion injury: where do we stand?Position Paper from the Working Group of Cellular Biology of the Heart of the European Society of Cardiology

Ovize, M; Baxter, GF; Di Lisa, F; Ferdinandy, P; Garcia-Dorado, D; Hausenloy, DJ; Heusch, G; ... Schulz, R; + view all (2010) Postconditioning and protection from reperfusion injury: where do we stand?Position Paper from the Working Group of Cellular Biology of the Heart of the European Society of Cardiology. CARDIOVASC RES , 87 (3) 406 - 423. 10.1093/cvr/cvq129.

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Abstract

Ischaemic postconditioning (brief periods of ischaemia alternating with brief periods of reflow applied at the onset of reperfusion following sustained ischaemia) effectively reduces myocardial infarct size in all species tested so far, including humans. Ischaemic postconditioning is a simple and safe manoeuvre, but because reperfusion injury is initiated within minutes of reflow, postconditioning must be applied at the onset of reperfusion. The mechanisms of protection by postconditioning include: formation and release of several autacoids and cytokines; maintained acidosis during early reperfusion; activation of protein kinases; preservation of mitochondrial function, most strikingly the attenuation of opening of the mitochondrial permeability transition pore (MPTP). Exogenous recruitment of some of the identified signalling steps can induce cardioprotection when applied at the time of reperfusion in animal experiments, but more recently cardioprotection was also observed in a proof-of-concept clinical trial. Indeed, studies in patients with an acute myocardial infarction showed a reduction of infarct size and improved left ventricular function when they underwent ischaemic postconditioning or pharmacological inhibition of MPTP opening during interventional reperfusion. Further animal studies and large-scale human studies are needed to determine whether patients with different co-morbidities and co-medications respond equally to protection by postconditioning. Also, our understanding of the underlying mechanisms must be improved to develop new therapeutic strategies to be applied at reperfusion with the ultimate aim of limiting the burden of ischaemic heart disease and potentially providing protection for other organs at risk of reperfusion injury, such as brain and kidney.

Type: Article
Title: Postconditioning and protection from reperfusion injury: where do we stand?Position Paper from the Working Group of Cellular Biology of the Heart of the European Society of Cardiology
DOI: 10.1093/cvr/cvq129
Keywords: Postconditioning, Ischaemia, Reperfusion, ACUTE MYOCARDIAL-INFARCTION, MITOCHONDRIAL PERMEABILITY TRANSITION, PERCUTANEOUS CORONARY INTERVENTION, NECROSIS-FACTOR-ALPHA, BRADYKININ B-2 RECEPTORS, SENSITIVE K+ CHANNEL, BRIEF RENAL ISCHEMIA, ISOLATED RAT HEARTS, ADENOSINE RECEPTORS, IN-VIVO
UCL classification: UCL > Provost and Vice Provost Offices
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Pop Health Sciences > Institute of Cardiovascular Science
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Pop Health Sciences > Institute of Cardiovascular Science > Pre-clinical and Fundamental Science
URI: http://discovery.ucl.ac.uk/id/eprint/118609
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