نتایج جستجو برای: myocardial ischaemia reperfusion injury
تعداد نتایج: 470209 فیلتر نتایج به سال:
Endothelial dysfunction is an essential deleterious modulator of ischaemia/reperfusion (I/R) injury. Secretory leukocyte protease inhibitor (SLPI) has demonstrated myocardial protection in cardiac transplantation; however, the effect of SLPI in endothelial I/R injury remains unexplored. In the present study, the effect of recombinant human SLPI (rhSLPI) treatment against endothelial cells (ECs)...
AIMS Coronary artery occlusion resulting in ischaemia/reperfusion (I/R) injury is a major cause of mortality in the western world. Circulating natural IgM has been shown to play a significant role in reperfusion injury, leading to the notion of a pathogenic response against self by the innate immune system. A specific self-antigen (non-muscle myosin heavy chain II) was recently identified as th...
BACKGROUND Remote ischaemic preconditioning (RIPC) induced by brief ischaemia and reperfusion of the arm reduces myocardial injury in coronary artery bypass (CABG) surgery patients receiving predominantly cross-clamp fibrillation for myocardial protection. However, cold-blood cardioplegia is the more commonly used method world wide. OBJECTIVE To assess whether RIPC is cardioprotective in CABG...
We have investigated if fentanyl protects against myocardial ischaemic injury and if so, if the mechanism of this protection is mediated via opioid and adenosine A1 receptors, and KATP channels. Langendorff rat hearts were subjected to global ischaemia (30 min) and reperfusion (60 min). The drugs were administered before induction of ischaemia and maintained throughout the experiment. Treatment...
This study investigated the protective effects of carvedilol, a potent antioxidant, in a rat model of tourniquet-induced ischaemia-reperfusion injury of the hind limb. Thirty rats were divided equally into three groups: the control group (group 1) was only anaesthetized, without creating an ischaemia-reperfusion injury; group 2 was submitted to ischaemia (4 h), followed by a 2-h reperfusion per...
Myocardial ischaemia–reperfusion (I/R) injury is a well-known term for exacerbation of cellular destruction and dysfunction after the restoration blood flow to previously ischaemic heart. A vast number studies that have demonstrated role mineralocorticoids in cardiovascular diseases based on use pharmacological mineralocorticoid receptor (MR) antagonists. This review paper aimed summarize curre...
BACKGROUND AND AIMS Injuries caused by ischaemia and ischaemia/reperfusion in the small intestine have been widely accepted as resulting in necrosis. The aim of this study was to ascertain whether apoptosis also occurs. METHODS Intestinal epithelium from rats subjected to ischaemia (15-90 minutes) and ischaemia/reperfusion (15 minutes ischaemia followed by 15-75 minutes of reperfusion) was st...
A specific action against myocardial reperfusion injury of the oxygen paradox type was recently characterized for halothane after anoxic perfusion in isolated rat hearts and isolated cardiomyocytes. In this study, we have characterized the protective effects of the clinically available inhalation anaesthetics during reperfusion after ischaemia. In isolated, isovolumically beating rat hearts per...
BACKGROUND A better understanding of the pathophysiology of ischaemia-reperfusion injury and a possible treatment for it, is of great importance. The deep inferior epigastric perforator (DIEP) flap is an innovative, clinical model of ischaemia-reperfusion. There has been an ongoing interest in the health benefits and medical applications of antioxidants. We hypothesised that during ischaemia-re...
AIMS The response of the myocardium to an ischaemic insult is regulated by two highly homologous protein kinase C (PKC) isozymes, delta and epsilonPKC. Here, we determined the spatial and temporal relationships between these two isozymes in the context of ischaemia/reperfusion (I/R) and ischaemic preconditioning (IPC) to better understand their roles in cardioprotection. METHODS AND RESULTS U...
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