Haemodynamic and coronary effects of quazodine in cats with developing myocardial infarcts

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Abstract
Acute ligation of the descending branch of the left coronary artery in anaesthetized cats resulted, within 1–2 h, in a 30% decrease in local blood flow in the region mainly supplied by the ligated vessel, a fall in systemic blood pressure, in cardiac output, and in left ventricular dP/dt max (LVdP/dt). There was electrocardiographic evidence of myocardial ischaemia (pronounced ST elevation). In these animals with developing myocardial infarcts, intravenous infusions of quazodine (MJ1988; 6,7-dimethoxy-4-ethyl-quinazoline) markedly increased myocardial contractility and local myocardial blood flow in the developing infarct, and decreased systemic arterial pressure, peripheral vascular resistance and left ventricular end-diastolic pressure, effects similar to those observed in normal cats. The increase in cardiac contractility (cardiac output and LVdP/dt) occurred without a concomitant increase in myocardial metabolic heat production. This ‘oxygen sparing effect’ probably results from a decrease in left ventricular wall tension. It is suggested that quazodine warrants further investigation as a cardiac stimulant in power failure following myocardial infarction in man.