Objective(s): Reperfusion of ischaemic myocardium results in reduced nitric oxide (NO) biosynthesis by endothelial nitric oxide synthase (eNOS) leading to endothelial dysfunction and subsequent tissue damage. Impaired NO biosynthesis may be partly due to increased levels of asymmetrical dimethylarginine (ADMA), an endogenous inhibitor of eNOS. As dimethylarginine dimet...

Apoptosis is a crucial event that can initiate ischaemia-reperfusion induced inflammation and subsequent tissue injury. Myocardial ischaemia reperfusion is associated with activation of intracellular death proteases known as calpains. Myocardial ischaemia was induced in isolated rat heart which was subjected to 30 min ischaemia followed by reperfusion for 120min. The effect of calpain inhibitor...

The myocardial injury that occurs following a period of ischaemia and reperfusion is well recognised and the underlying mechanisms have been extensively investigated in healthy myocardial tissues; however, the influence of the risk factors associated with cardiovascular diseases on ischaemia/reperfusion injury remains unclear. In this article, the present knowledge on how clinical pathologies s...

1. To recognise that acute myocardial ischaemia/reperfusion injury is a neglected therapeutic target for cardioprotection that is responsible for the ongoing morbidity and mortality of patients with ischaemic heart disease. 2. To be aware that cardiac bypass surgery and STEMI are the major clinical settings in which the heart is subjected to acute ischaemia/reperfusion injury. 3. To be familiar...

BACKGROUND In patients with acute myocardial infarction, restoration of coronary flow by primary coronary intervention (PCI) can lead to profound ischaemia-reperfusion injury with detrimental effects on myocardial salvage. Non-invasive assessment of interstitial myocardial haemorrhage by T2* cardiac MRI (T2*-CMR) provides a novel and specific biomarker of severe reperfusion injury which may be ...

AIMS Intravascular inflammatory events during ischaemia/reperfusion injury following coronary angioplasty alter and denudate the endothelium of its natural anticoagulant heparan sulfate proteoglycan (HSPG) layer, contributing to myocardial tissue damage. We propose that locally targeted cytoprotection of ischaemic myocardium with the glycosaminoglycan analogue dextran sulfate (DXS, MW 5000) may...

Aims Intravascular inflammatory events during ischaemia/reperfusion injury following coronary angioplasty alter and denudate the endothelium of its natural anticoagulant heparan sulfate proteoglycan (HSPG) layer, contributing to myocardial tissue damage. We propose that locally targeted cytoprotection of ischaemic myocardium with the glycosaminoglycan analogue dextran sulfate (DXS, MW 5000) may...

OBJECTIVES Previous studies have suggested that failure of the synthesis of nitric oxide is involved in the pathophysiology of myocardial ischaemia-reperfusion injury. In this study, we investigated the effect of mebudipine, a new dihydropyridine calcium channel blocker, on cardiac function and activity of the myocardial nitric oxide system in ischaemia-reperfusion injury in isolated rat hearts...

AIMS Several intracellular mediators have been implicated as new therapeutic targets against myocardial ischaemia and reperfusion injury. However, clinically effective salvage pathways remain undiscovered. Here, we focused on the potential role of the adaptor protein p66(Shc) as a regulator of myocardial injury in a mouse model of cardiac ischaemia and reperfusion. METHODS AND RESULTS Adult m...

Ipratropium bromide, a nonselective muscarinic antagonist, is widely prescribed for the treatment of chronic obstructive pulmonary disease (COPD). Analyses of COPD patients, with underlying ischaemic heart disease, receiving anticholinergics, have indicated increased risk of severity and occurrence of cardiovascular events (including myocardial infarction). The present study explored whether ip...