The haemodynamic effects of a single dose of intravenous molsidomine were assessed in 12 patients with severe coronary disease. The investigation was carried out at rest during angina induced by pacing and after molsidomine during pacing at the rate at which angina had been produced. During angina, left ventricular systolic and end-diastolic pressure rose, left ventricular stroke work fell and coronary flow and myocardial oxygen consumption increased by 58.3% above the control levels. After the administration of molsidomine, atrial stimulation was not followed by angina and there were no significant changes in systolic blood pressure. Left ventricular end-diastolic pressure fell sharply and coronary flow and myocardial oxygen consumption were only 38% and 33% higher, respectively, than the control levels. The beneficial effects of molsidomine in ischaemic heart disease, therefore, are the result of peripheral vasodilation which, by reducing the preload and afterload, lowers the oxygen requirements of the myocardium and thus increase the threshold for angina. A direct action on the coronary network can not be excluded but if such an action does exist it must be very small in the light of the marked systemic effect.