Intra-myocardial hemorrhage and cardiac microvascular injury in ischemia/reperfusion. A systematic review of current evidences.

The 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.

The β-adrenergic receptor agonist formoterol attenuates necrosis and apoptosis in the rat myocardium under experimental stress-induced cardiac injury.

Background: 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.

δ-Opioid Receptor as a Molecular Target for Increasing Cardiac Resistance to Reperfusion in Drug Development.

An analysis of published data and the results of our own studies reveal that the activation of a peripheral δ-opioid receptor (δ-OR) increases the cardiac tolerance to reperfusion. It has been found that this δ-OR is localized in cardiomyocytes. Endogenous opioids are not involved in the regulation of cardiac resistance to reperfusion.

Do reactive oxygen species damage or protect the heart in ischemia and reperfusion? Analysis on experimental and clinical data.

The role of reactive oxygen species (ROS) in ischemic and reperfusion (I/R) injury of the heart has been discussed for more than 40 years. It has been demonstrated that reperfusion triggers a multiple increase in free radical generation in the isolated heart. Antioxidants were found to have the ability to mitigate I/R injury of the heart.

Decrease in Infarct-Limiting Effect of Chronic Normobaric Hypoxia in Rats with Induced Metabolic Syndrome Is Associated with Disturbances of Carbohydrate and Lipid Metabolism.

We studied the infarct-limiting effect of adaptation to chronic normobaric hypoxia in rats with induced metabolic syndrome and the relationship between disturbances of adaptive cardioprotection and disorders of carbohydrate and lipid metabolism. Adaptation to chronic normobaric hypoxia was carried out for 21 days at 12% O and 0.3% CO.