Electrophysiologically guided surgical procedures for the ablation of supraventricular and ventricular dysrhythmias often require prolonged periods of tachycardia to complete intraoperative mappingg studies. It is unknown whether tachycardia depletes the myocardium of high-energy compounds or alters subsequent tolerance to ischemia. In the present study, 12 anesthetized dogs were paced from the right ventricle at a cycle length of 250 msec for 60 minutes. In seven animals, drill biopsy specimens were taken from the left ventricular free wall for analysis of adenine nucleotide levels and their breakdown products before and after pacing and after 20 minutes of recovery from pacing. In the remaining five animals, the heart was made totally ischemic immediately after tachycardia and the time to the onset of ischemic contracture was determined and compared to that of five nonpaced control dogs. Acute tachycardia resulted in no significant reduction in adenine nucleotide levels compared to control values. Furthermore, in hearts rendered totally ischemic after tachycardia, the mean time to ischemic contracture was 65.6 ± 1.3 minutes versus 63.6 ± 2 minutes in nonpaced control animals (no significant difference). These data show that pacing-induced tachycardia in the normal heart does not decrease adenine nucleotide levels or affect subsequent tolerance to ischemia. These results may be clinically relevant to patients without coronary artery disease who undergo operative procedures necessitating prolonged periods of tachycardia for intraoperative mapping to identify the site of arrhythmogenesis.