In the early phase of acute myocardial infarction, timely reperfusion is a prerequisite to contain the extent of cellular and vascular injury. In the absence of reperfusion, severe ischaemia inevitably leads to myocardial necrosis involving all of the area at risk. Early reperfusion may prevent the death of ischaemic cardiomyocytes and is the therapeutic strategy of choice in patients with acut...

UNLABELLED Androgenic anabolic steroids (AAS) are often used by athletes to enhance athletic performance but are strongly associated with detrimental cardiovascular effects including sudden cardiac death. HYPOTHESIS AAS use increases myocardial susceptibility to ischaemia/reperfusion injury. METHODS Rats were trained (swimming) with or without intramuscular injection of nandrolone laurate (...

Ischaemic preconditioning was originally described in animal hearts as histological infarct-size limitation by a previous brief episode of ischaemia. In humans, ischaemic preconditioning has been demonstrated in several in vitro and in vivo models, including coronary artery bypass grafting and percutaneous transluminal coronary angiograplasty, using surrogate markers of ischaemia and reperfusio...

BACKGROUND Nitric oxide (NO) plays a vital role in vascular homeostasis and in the pathophysiology of coronary heart disease. Its metabolites, nitrite and nitrate, have vasculoprotective properties, whereas peroxynitrite, an oxidant metabolite of NO, is cytotoxic and can aggravate myocardial damage during ischaemic reperfusion injury. Peroxynitrite nitrates free and protein bound tyrosine resid...

Enzyme release by ischaemic myocardium has been used as a hallmark of the infarction process for several decades: in the clinical setting, deterioration of cell membrane integrity, as evidenced by the release of macromolecules such as creatine kinase and lactate dehydrogenase, has been used as quantitative indication of myocardial infarction. Leakage of membrane-impermeable molecules due to sar...