Effects of a protocol of ischemic postconditioning

Authors: Claudia Penna Francesca Tullio Francesca Moro Anna Folino Annalisa Merlino Pasquale Pagliaro

Publish Date: 2009/12/13

Volume: 105, Issue: 2, Pages: 181-192

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Abstract

Brief periods a few seconds of cyclic coronary occlusions applied early in reperfusion induce a cardioprotection against infarct size called postconditioning PostC in which B2bradykinin receptors play a pivotal role Since angiotensinconverting enzyme ACE inhibitors reduce degradation of kinins we studied the effects of PostC on infarct size and postischemic myocardial dysfunction in both normotensive WKY and spontaneously hypertensive rats SHR acutely or chronically treated with the ACE inhibitor Captopril Isolated hearts from SHR and WKY rats were subjected to the following protocols a ischemia for 30 and 120min reperfusion I/R b I/R + PostC protocol 5cycles 10s I/R c pretreatment with Captopril for 4weeks before to subject the hearts to I/R with or without PostC maneuvers Some SHR hearts were treated with Captopril during the 20 or 40min early reperfusion with or without PostC maneuvers Cardiac function was assessed in vivo with echocardiography Left ventricular pressure and infarct size were measured ex vivo Chronic Captopril significantly reduced left ventricular hypertrophy in SHR and reduced infarct size in both WKY and SHR hearts PostC maneuvers significantly reduced infarct size in WKY but not in SHR hearts Yet PostC slightly improved postischemic systolic function in untreated SHR Captopril given in reperfusion was unable to limit I/R injury in SHR hearts Data show that PostC protection against infarct size is blunted in SHR and that PostC is unable to add its protective effect to those of chronic Captopril which per se reduces cardiac hypertrophy and heart susceptibility to I/R insult

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