Myocardial protection from ischemia/reperfusion injury


Ischemic heart disease and its major clinical form, myocardial infarction, are widespread and are the leading causes of death in most developed countries. Time factor is essential for successful treatment of the myocardial infarction. However, surgical or medical interventions aimed at the rapid restoration of blood supply to ischemic tissues, including stenting of injured arteries or thrombolysis, may not always be done in the shortest possible time. In this respect, maintenance of increased tissue resistance to ischemia is necessary in some cases, thereby increasing the time period during which myocardial revascularization will be clinically significant. These approaches are the basis of modern concepts of cardioprotection. The research in the field of myocardial protection is translational by the type. In 2013, researchers of the Almazov Centre are carried out a multicenter randomized clinical trial of the effectiveness of ischemic postconditioning in patients with combined aortic valve and ascending aorta disease underwent cardiac surgery with extracorporeal circulation. Earlier experimental studies have provided the background for the present clinical studies on cardioprotective effect of remote and pharmacological preconditioning.

The processes of programmed cell death (apoptosis, necroptosis, autophagy) are central to the pathogenesis of ischemic, and in particular, reperfusion injury of the myocardium and brain. In recent years, there has been increased attention to the study of pharmacological modulators of programmed cell death. In 2005, a new type of cell death, called necroptosis, which can be suppressed by the inhibitors, called necrostatins, was described for the first time. Current experimental studies carried out by researchers of the Institute are aimed at cardioprotective effects of necrostatins-1, -5, and -7, specific inhibitors of necroptosis, on a model of ischemia/reperfusion injury in isolated rat hearts, as well as on a model of permanent coronary artery occlusion and regional myocardial ischemia/reperfusion in vivo.