Abstract
Hypothalamic proline-rich peptide-1 (PRP-1), a neurosecretory cytokine appeared to be involved in the multiple mechanisms of cardioprotection. Dose-dependent effects of PRP-1 (4 and 8 µg) were studied in an open-chest model of myocardial ischemia-reperfusion injury (IRI). Adult mail Sprague Dawley rats underwent 40-minute left anterior descending coronary artery occlusion, under isoflurane anesthesia followed by 2 and/or 24 h of reperfusion. Groups treated with PRP-1 were compared to control and it has been revealed that the efficient dose of PRP-1 can restore in a time-dependent manner the contractile activity of the myocardium and suppress the both inflammation and necrosis via amelioration of oxidative stress in the cardiac tissues there through contributing to the in vivo reduction of myocardial infarct volume and an improvement the cardiac hemodynamics and coronary circulation. New studies are needed to ascertain a beneficial effect of PRP-1 in humans and its future clinic use for the myocardial IRI treatment.
Highlights
IntroductionThe process of restoring blood flow to the ischemic myocardium is the most efficient way of prevention the deleterious impact of pathogenic factors associated with myocardial ischemia, to reduce the size of a myocardial infarct and improve the clinical outcome.[1] the beneficial effects of myocardial reperfusion are reduced because of the development of ischemiareperfusion injury (IRI) that leads to arrhythmia, myocardial stunning (the reversible reduction of function of heart contraction after reperfusion), overproduction of reactive oxygen species (ROS)
Reperfusion, the process of restoring blood flow to the ischemic myocardium is the most efficient way of prevention the deleterious impact of pathogenic factors associated with myocardial ischemia, to reduce the size of a myocardial infarct and improve the clinical outcome.[1]
The beneficial effects of myocardial reperfusion are reduced because of the development of ischemiareperfusion injury (IRI) that leads to arrhythmia, myocardial stunning, overproduction of reactive oxygen species (ROS). It is accompanied by necrosis apoptosis, and autophagy is contributing to the death of cardiomyocytes viable before myocardial reperfusion.[2,3]
Summary
The process of restoring blood flow to the ischemic myocardium is the most efficient way of prevention the deleterious impact of pathogenic factors associated with myocardial ischemia, to reduce the size of a myocardial infarct and improve the clinical outcome.[1] the beneficial effects of myocardial reperfusion are reduced because of the development of ischemiareperfusion injury (IRI) that leads to arrhythmia, myocardial stunning (the reversible reduction of function of heart contraction after reperfusion), overproduction of reactive oxygen species (ROS).
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