Protective effects of adenosine on acute myocardial ischemia

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Adult mongrel dogs were anesthetized with pentobarbital and enflurane in air. A hydraulic snare was applied over the left anterior descending artery to make a critical stenosis. In the hypotensive period, adenosine 100 mcg/kg/min was infused. Blood pressure was significantly decreased with a significant decrease in systemic vascular resistance (SVR). Cardiac output was increased with no change in Emax. When adenosine was given during myocardial ischemia, cardiac output, Emax were better maintained in adenosine-treated dogs than in the control group. After completion of the 60 min of ischemic period, the heart was excised and resected in ischemic and non-ischemic areas. The intracellular concentrations of adenosine, adenosine diphosphate, adenosine triphosphate, and beta-receptor density on the myocytes were measured using HPLC and H3-dihydroalprenol (DHA) binding assay respectively. There were no significant differences in high-energy phosphates concentrations and beta-receptor density between adenosine-treated myocardium and the control myocardium.The results suggested that adenosine preserved the myocardial pump function secondary to the decreased afterload in acute ischemic heart. Preservation of the intracellular high-energy phosphates and beta-receptor density probably did not play an important role to maintain cardiac systolic function in this canine model.