The effect of the selective μ-opioid receptor agonist endomorphin-1 in reperfusion injury in male Wistar rats was studied in vivo and in vitro. The in vivo experiment included coronary artery occlusion (45 min) and reperfusion (120 min); in in vitro experiments, 45-min global ischemia of the isolated rat heart was followed by 30-min reperfusion. Endomorphin-1 was administered intravenously 5 min before in vivo reperfusion (at a dose 50 μg/kg) or added to the perfusion solution at the onset of reperfusion of the isolated heart (in a concentration of 152 nmol/liter).
View Article and Find Full Text PDFThe in-hospital mortality rate in acute myocardial infarction (AMI) remains high despite the undoubted achievements in treatment of this disease achieved in the last 40 years. The dangerous complications of AMI remain cardiac microvascular injury (CMI) and intramyocardial hemorrhage (IMH). IMH is a widespread pathology that occurs in 42 - 57% of patients with ST-segment elevation myocardial infarction and percutaneous coronary intervention.
View Article and Find Full Text PDFMicrovascular obstruction (MVO) of coronary arteries promotes an increase in mortality and major adverse cardiac events in patients with acute myocardial infarction (AMI) and percutaneous coronary intervention (PCI). Intramyocardial hemorrhage (IMH) is observed in 41-50% of patients with ST-segment elevation myocardial infarction and PCI. The occurrence of IMH is accompanied by inflammation.
View Article and Find Full Text PDFStudies assessing the treatment of refractory no-reflow in patients with ST-elevation myocardial infarction (STEMI) are limited to clinical cases and pilot studies. This study aimed to evaluate the efficacy and safety of intracoronary adrenaline administration in such patients. Ninety consecutive patients with refractory coronary no-reflow during percutaneous coronary intervention (PCI) were prospectively included after the initial failure of conventional treatment.
View Article and Find Full Text PDFBackground: Currently, there is no effective therapy for takotsubo syndrome (stress-induced cardiac injury in humans) in the clinics. It has previously been shown that β-adrenergic receptor (β-AR) agonist formoterol reduces cardiomyocyte injury in experimental takotsubo syndrome.
Objectives: The aim of this study was to investigate whether formoterol prevents apoptosis and necrosis of cardiomyocytes and endothelial cells in stress-induced cardiomyopathy.