After an initial perfusion using the Langendorff technique, rat hearts were perfused through the left atrium according to the working heart technique. Hearts were preloaded with l noradrenaline 3H (3H-NA) and the release of radioactivity and 3H-NA in the coronary effluent was evaluated. Coronary flow, cardiac output, myocardial oxygen consumption and the electrocardiogram were simultaneously recorded. The perfusion medium consisted of a modified Krebs Henseleit solution containing 3 mM potassium and 0.5 mM sodium palmitate complexed with serum albumin in a molar ratio of 6/1. 1. The addition of palmitate to the perfusion fluid during the Langendorff perfusion produced increases in coronary flow and oxygen consumption, but the release of 3H-NA was not significantly modified, and no irregularities in ventricular concentration were observed. Likewise, the working of the heart did not alter the rate of 3H-NA release. 2. Ischemia was induced on the working heart by left coronary artery ligation for 15 min. It resulted in a reduction in coronary flow and in a similar decrease in the rate of release of 3H-NA. During the first minutes of the occlusion period, there was a slight increase in the incidence of ventricular extrasystoles, but ventricular tachycardia or fibrillation were never encountered. 3. Re-perfusion was accompanied by the occurrence of ventricular tachycardia and fibrillation in all the hearts. These arrhythmias were almost uninterrupted during the first 3 min of re-perfusion, and lasted to a lesser extent up to the 9th minute. Re-perfusion resulted in a sudden release of 3H-NA which was multiplied by a factor 4 during the first 2 min, and then decreased progressively. 4. These results suggest that a release of NA from the myocardial ischemic zones plays a role in the genesis of cardiac arrhythmias following reperfusion.