Effects of intravenous nifedipine on the ischemic myocardium of dogs subjected to coronary ligation were evaluated with a newly developed myothermal technique. Sensitive, fast-reacting miniature thermistors implanted within the ventricular wall were used in conjunction with low noise thermistor bridges to monitor beat-to-beat intramyocardial heat pulses and to detect intramyocardial cold transients after mechanized injections of cold saline into the left atrium. Myocardial ischemia reduced the amplitude of the pulse signals and decreased mean intramyocardial temperature. Ischemia also reduced the amplitude of the intramyocardial cold transients detected after injection of cold saline solution. All thermal changes due to ischemia were partly reversed by nifedipine. The amplitude of the cold signals correlated positively (r = 0.85) with local myocardial perfusion estimated by the radioactive microsphere technique. Thus, estimates of local perfusion by two independent techniques confirmed that nifedipine increased collateral perfusion. In addition, simultaneous measurements of peripheral coronary pressure indicated that the drug decreased resistance in the coronary bed distal to the occlusion. Ultrasonic measurements of myocardial segment length revealed that nifedipine improved myocardial shortening in ischemic zones, a response that accounts for the nifedipine-induced increases in local heat. Thus, the results show that nifedipine increases collateral flow to the acutely ischemic myocardium and that improved perfusion is accompanied by enhanced contractile performance. These findings also indicate that the protective action of nifedipine on ischemic myocardium is not predominantly mediated by a cardioplegic effect limiting the metabolic needs of the myocardium at risk.