Dihydroergotoxine, an ergot alkaloid without marked hypotensive effect, improves blood flow and metabolism in the underperfused canine myocardium.

Regional myocardial blood flow was assessed in 6 anaesthetized dogs using radiolabelled microspheres. Lactate, H+, and O2 content were measured in arterial and local venous blood, obtained from the area supplied by the circumflex branch of the left coronary artery (LCX). Constriction of LCX by 67% led to considerable hemodynamic changes indicative of depressed global myocardial function. A significant release of lactate from the underperfused part of the left ventricle was recorded. Infusion of 0.7 micrograms/kg dihydroergotoxine over a period of 5 min induced a decrease in heart rate, left ventricular dp/dt max, and cardiac output, a sustained increase in total peripheral and femoral resistance and a transient increase in mean arterial blood pressure. Dihydroergotoxine markedly reduced lactate release and even, in some cases, induced lactate uptake and led to a significant increase in the endocardial blood flow both in the underperfused and normally perfused left ventricle. It is concluded that dihydroergotoxine, due to its ability to reduce myocardial oxygen demand and owing to its alpha-sympatholytic activity, which is not accompanied by any marked decrease in arterial blood pressure, causes improvement in blood flow in the underperfused myocardium and a marked amelioration of the impaired metabolic processes.