Adenosine exacerbates ischemic myocardial injury during regional coronary hypoxemia in the dog.

To investigate the myocardial protective effect of adenosine (ADO), the left anterior descending artery of 10 dogs was cannulated and perfused at a pressure of 100 mmHg. Hypoxic coronary perfusion was conducted for 60 min followed by 60 min of normoxic reperfusion (group 1, control, n = 5). In group 2 (n = 5), ADO was continuously infused at a rate of 40 micrograms/kg/min for 30 min before and during 60 min of hypoxic blood perfusion and for 60 min following normoxic reperfusion. In group 1, R wave amplitude and TQ segment of the epicardial surface electrocardiogram (EPIECG) were reduced, the ST segment was elevated, and a new Q wave developed during hypoxic blood perfusion. However, at 60 min of normoxic reperfusion, the R wave amplitude recovered to approximately 60% of its control value. Also, ST segment elevation was restored to normal and the new Q wave disappeared. The TQ segment returned to normal after approximately 20 min of hypoxic perfusion. Histological analysis showed myocardial infarction in the subendocardium, but not in the subepicardium. In group 2, EPIECG findings during hypoxic blood perfusion were similar to those observed in group 1. However, the recovery of ST segment elevation during normoxic reperfusion was slower than that observed in group 1. R wave restoration did not occur in group 2. Furthermore, the new Q wave remained present throughout the normoxic reperfusion period. Transmural infarction and severe congestion were observed histologically in this group. Obvious contraction bands were not demonstrated histologically in either group. These findings suggest that ADO did not protect myocardial viability during 60 min of hypoxic blood perfusion, but instead, ADO exacerbated ischemic injury during regional hypoxic perfusion.