Preconditioning the heart with brief periods of ischaemia induces delayed endothelial protection against reperfusion injury, but the precise mechanisms involved in this endogenous protein are still unclear. Induction of the type II-nitric oxide synthase (iNOS) acts as a mediator of the preconditioning against myocardial infarction and stunning. The present study was designed to assess whether i...

Background Myocardial ischaemia-reperfusion injury is a major cause of mortality and morbidity in the developed world. Many approaches have been investigated to counteract the pathological consequences associated with acute myocardial infarction (AMI) and cardiac remodelling. It is accepted that inflammation, and therefore activation of the complement pathway, is a crucial step in the pathogene...

AIMS Innate immune and inflammatory responses are involved in myocardial ischaemia/reperfusion (I/R) injury. The interleukin-1 receptor (IL-1R)-mediated, MyD88-dependent nuclear factor kappa B (NF-kappaB) activation pathway plays an important role in the induction of innate immunity and inflammation. However, the role of the IL-1R-MyD88 pathway in myocardial I/R injury has not been thoroughly i...

myocardial ischemia (mi) resulting in infarction is an important cause of mortality and morbidity worldwide. acute ischaemia rapidly impairs myocardial contractile function. myocardial dysfunction persisting for several hours after transient non-lethal ischaemia, eventually resulting in full functional recovery is termed as myocardial stunning. hibernation is now thought to be the consequence o...

Leucocytes have been shown to play a fundamental role in the pathophysiology of inflammation. This prospective, randomized, controlled study was designed to identify the most advantageous leucocyte depletion technique in terms of reduction in systemic inflammatory response syndrome and myocardial ischaemia reperfusion injury associated with cardiopulmonary bypass (CPB). Forty consecutive patien...

Ischemic Heart Disease (IHD) is the main global cause of death. Previous studies indicated that recombinant human secretory leukocyte protease inhibitor (rhSLPI) exhibits a cardioprotective effect against myocardial ischaemia/reperfusion (I/R) injury. However, SLPI has short half-life in vivo due to digestion by enzymes circulation. The application nanoparticle encapsulation could be beneficial...

The efficacy of 2,3-butanedione monoxime (BDM) as additive to St. Thomas Hospital II solution (STH) as compared to initial BDM reperfusion with regard to myocardial ischaemia/reperfusion injury was investigated in isolated guinea pig hearts. Isolated guinea pig hearts were perfused with Krebs-Henseleit buffer in the Langendorff technique at constant pressure of 55 mmHg. After cardioplegic arres...

AIMS Thrombomodulin (TM), via its lectin-like domain (LLD), exhibits anti-inflammatory properties partly by sequestering the pro-inflammatory cytokine, high-mobility group box 1 (HMGB1). Since myocardial damage after ischaemia and reperfusion is mediated by inflammation, we evaluated the cardioprotective effects of the LLD of TM. Using an in vivo mouse model of transient ischaemia and in vitro ...

1. Sandanger Ø, Ranheim T, Vinge LE, Bliksøen M, Alfsnes K, Finsen AV et al. The NLRP3 inflammasome is up-regulated in cardiac fibroblasts and mediates myocardial ischaemia-reperfusion injury. Cardiovasc Res 2013;99: 164–174. 2. Mezzaroma E, Toldo S, Farkas D, Seropian IM, Van Tassell BW, Salloum FN et al. The inflammasome promotes adverse cardiac remodeling following acute myocardial infarctio...

1. Sandanger Ø, Ranheim T, Vinge LE, Bliksøen M, Alfsnes K, Finsen AV et al. The NLRP3 inflammasome is up-regulated in cardiac fibroblasts and mediates myocardial ischaemia-reperfusion injury. Cardiovasc Res 2013;99: 164–174. 2. Mezzaroma E, Toldo S, Farkas D, Seropian IM, Van Tassell BW, Salloum FN et al. The inflammasome promotes adverse cardiac remodeling following acute myocardial infarctio...