Receptor-Mediated and Metabolic Effects of Adenosine in Ischemic and Postischemic Myocardium

摘要: Myocardial ischemia is associated with rapid decreases in cardiac contractility and the high-energy phosphates creatine phosphate (CrP) adenosine triphosphate (ATP). Ischemic durations of 20 minutes or less induce no cell necrosis, but upon reperfusion myocardium at risk exhibits prolonged contractile dysfunction, which may persist for hours to days. This postischemic depressed contractility, despite restoration normal coronary blood flow, defined as stunned myocardium. Longer are death, that is, myocardial infarction. Although exact mechanisms underlying ischemic/ injury not known, there substantial evidence purine nucleoside protects heart against both stunning infarction, part via activation sarcolemmal A1 receptors located on myocytes [1,2]. review will focus receptor-mediated metabolic effects ischemic attenuation ventricular dysfunction by adenosine.