AIMS Innate mechanisms of inter-organ protection underlie the phenomenon of remote ischaemic preconditioning (RPc) in which episode(s) of ischaemia and reperfusion in tissues remote from the heart reduce myocardial ischaemia/reperfusion injury. The uncertainty surrounding the mechanism(s) underlying RPc centres on whether humoral factor(s) produced during ischaemia/reperfusion of remote tissue ...

Platelets activated during experimental acute myocardial infarction (AMI) contribute to myocardial injury. This study aimed to investigate whether platelets from patients with AMI increase myocardial injury after ischaemia and reperfusion in isolated rat hearts and the modification of this effect by the P2Y12 receptor antagonist cangrelor and the glycoprotein IIb/IIIa receptor blocker abciximab...

2 Introduction It has been widely documented that plasma ET-1 and big ET-1 levels are increased in patients within a day of onset of acute myocardial infarction [1,2,3,4]. Similar changes in systemic plasma ET-1 are seen in animal models of myocardial ischaemia [5,6]. The source of the released ET-1 appears to be the area subjected to ischaemic damage, since in a study in anaesthetised pigs bot...

The pathogenesis of myocardial ischaemia/reperfusion injury is multifactorial. Understanding the mechanisms of myocardial ischaemia/reperfusion will benefit patients with ischaemic heart disease. Growth differentiation factor 11 (GDF11), a member of the secreted transforming growth factor-β superfamily, has been found to reverse age-related hypertrophy, revealing the important role of GDF11 in ...

The past few years have witnessed a remarkable advance in our understanding of the pathophysiology of coronary heart disease. Myocardial ischaemia usually occurs on the basis of coronary atherosclerosis. Although the functional consequences of depriving the myocardium of its blood supply have been appreciated for many years, the coronary heart disease is still the leading cause of morbidity and...

The concept that the reintroduction of oxygen to the ischaemic myocardium causes significant injury has long been known [1], and it is now well-established [2] that oxidative stress is one of the major initiators of myocardial injury during ischaemia and reperfusion. Cardiac surgery for coronary artery bypass generally involves cardiopulmonary bypass with cardioplegic arrest and elective global...

Myocardial ischaemia-reperfusion injury can be significantly reduced by an episode(s) of ischaemia-reperfusion applied prior to or during myocardial ischaemia (MI) to peripheral tissue located at a distance from the heart; this phenomenon is called remote ischaemic conditioning (RIc). Here, we compared the efficacy of RIc in protecting the heart when the RIc stimulus is applied prior to, during...

It seems surprising that more than five decades of intense biochemical and molecular research on a leading cause of death and disability globally—ischaemic myocardial injury/myocardial infarction—and the spending of huge sums of money have achieved relatively little in the prevention of cell death secondary to ischaemia. The greatest progress has been made in methods to mechanically or chemical...

Rapid restoration of blood flow has the greatest impact on reducing infarct size and improving patient prognosis in patients with ST-elevation myocardial infarction (MI). However, reperfusion itself can exacerbate myocardial damage on top of the initial ischaemic damage. Lethal reperfusion injury develops when sudden restoration of blood flow causes necrosis of myocytes that—albeit injured by t...