Improved lactate extraction in dogs with coronary artery ligation following administration of a thromboxane synthetase inhibitor.

Increased thromboxane A2 formation has been implicated in the pathophysiology of acute myocardial ischemia. The present study was designed to investigate the action of imidazole, a thromboxane synthetase inhibitor, during acute myocardial ischemia induced in anesthetized dogs. Regional ischemia was produced by ligation of the left anterior descending coronary artery (LAD), which caused a decrease in myocardial lactate extraction across the ischemic area, decreases in myocardial high energy phosphate contents and an increase in myocardial lactate in the center of the ischemic region. Intravenous administration of imidazole prior to LAD ligation attenuated the decrease in myocardial lactate extraction, but did not alter the depression in high energy phosphates or the rise in myocardial lactate content in the center of the ischemic myocardium. The results of this study support the suggested protective action of imidazole during an ischemic insult; perhaps by maintaining the metabolic status of the moderately ischemic border zone.