The importance of nitric oxide bioavailability and endothelial mechanisms for cardioprotection by pharmacological intervention during myocardial ischaemia and reperfusion

TL;DRAbstract

<p>Myocardial ischaemia initiates complex severe cellular changes and, after a critical time period, myocardial cell death. Despite that restitution of coronary blood flow is an absolute pre-requisite for tissue survival, myocardial reperfusion per se will also increase irreversible damage in the jeopardised myocardium. Endothelial dysfunction is an early event during ischaemia and reperfusion, which is characterised by an impairment of endothelium-dependent relaxations, mainly due to reduced nitric oxide (NO) bioavailability and increased production of endothelin-1 (ET-1). Certain ET-1 receptor antagonists and calcium channels blockers may in addition to their classical actions, affect NO bioavailability.</p><p>The aim of the studies was to investigate the involvement and mechanisms of the endothelial factors NO and ET-1 in the pathophysiology of myocardial ischaemia-reperfusion damage. Of particular interest was the importance of NO bioavailability for the cardiopro

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