Since reperfusion early after acute myocardial infarction has been demonstrated to reduce the infarct size and mortality, many drugs and interventions to reduce the reperfusion injury have been tried with limited success. Adenosine, a potent coronary vasodilator, has been reported to counteract a few mechanisms implicated with reperfusion injury, however, its effects and exact mechanisms to reduce the reperfusion injury have not been clearly elucidated.

Effects of adenosine upon infarct size reduction and upon postulated mechanisms involved in the reperfusion injury such as no reflow phenomenon and neutrophil infiltration were evaluated in anesthetized open chest dog model where acute myocardial infarction was induced by 90 minute left anterior descending coronary artery occlusion followed by 240 minute reperfusion. Adenosine(3.75 mg/min) was administered intravenously for total 90 minutes from 30 minutes before reperfusion. Compared to control group(n=6), infarct area/risk area ratio was significantly lower in adenosine group(n=6)(34+12% vs. 22±11, p=0.04), although risk area/total left ventricular area ratio were similar in both groups. Myocardial blood flows(MBF), measured by radiolabelled microspheres, of the infarcted regions during coronary occlusion were similar in both groups, however, both subepicardial MBF(0.63±0.15ml/min/g vs. 0.95±0.31, p=0.02) and subendocardial MBF(0.45±0.08 ml/min/g vs. 0.69±0.27, p=0.02) were higher in daenosine group. Neutrophil infiltration, semiquantitatively measured under light microscope, were less severe in daenosine group,compared to control group.

Intravenous adenosine administered before coronary reperfusion appears to reduce infarct size by limiting reperfusion injury through improving no reflow phenomenon and preventing neutrophil infiltration to the ischemic myocardium during reperfusion.