Lack of thromboxane A2 involvement in the arrhythmias occurring during acute myocardial ischemia in dogs.

Coronary artery occlusion (CAO) followed by reperfusion of the ischemic myocardium has been associated with the onset of ventricular arrhythmias. It has been suggested that platelet aggregates in the ischemic area may release thromboxane A2 (TxA2) which may then be responsible for the arrhythmias that occur during reperfusion. To study this possibility, the effect of TxA2 synthetase inhibition on arrhythmias was examined in anesthetized dogs during occlusion and for 60 minutes following release. Imidazole (30 mg/kg) was infused intravenously for 10 minutes, followed by continuous infusion of 100 mg/kg/hr for 125 minutes. The left anterior descending coronary artery was occluded, 5 minutes after the initial dose, for 60 minutes. Three minutes after release of CAO, TxB2 concentrations were significantly higher in the arterial blood of vehicle-treated animals (2.06 +/- 0.53 pmoles/ml) than in either CAO + imidazole (0.66 +/- 0.16 pmoles/ml) or sham-CAO animals receiving imidazole (0.66 +/- 0.09 pmoles/l). However, CAO dogs whether receiving imidazole or 0.9% NaCl generated a significantly greater number of ectopic beats during and after occlusion than sham-CAO animals. Therefore, release of TxA2 does not appear to be a major causative factor in the generation of reperfusion arrhythmias in dogs following coronary artery occlusion.