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

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