Catecholamine-induced myocardial hypoxia in the presence of impaired coronary dilatability independent of external cardiac work

Surface electrocardiograms were taken in vagotomized cats over areas of the left ventricle. An adjustable nonoccluding restriction device prevented part of the coronary arterial supply from dilating. Under these circumstances, brief stimulation of the cardiac sympathetic nerves or reflex stimulation of the adreno-sympathetic system through electrically induced muscular “exercise,” or intravenous injection of catecholamines (epinephrine, norepinephrine) caused regularly marked elevations of the S-T segment and the T wave, even if concomitant augmentation of cardiac mechanical work was only minimal. Identical electrocardiographic changes were elicited by exogenous anoxia (breathing 100 per cent nitrogen), and by more complete coronary constriction. By contrast, no S-T displacement occurred despite coronary restriction when heavy work loads were imposed upon the heart by noncatecholamine influences, namely, tachycardia produced by electrical stimulation of the right atrium, or high rises of the blood pressure produced by intravenous injection of angiotensin II, or both combined. Neurogenic and blood-borne catecholamines cause severe regional myocardial hypoxia when the normal compensatory coronary dilatation is impaired. Such catecholamine-induced myocardial hypoxia is not caused by the concomitant augmentation of cardiac mechanical work which these neurohormones usually elicit, but by their specific biochemical oxygen-wasting properties. Our findings agree with the clinical experience that in patients with coronary sclerosis attacks of angina pectoris are ordinarily triggered by sympathetic-stimulating, catecholamine-liberating conditions (exercise, emotions and other stresses), and prevented by various antiadrenergic measures. Contrary to traditional belief, it is suggested that anginal symptoms do not occur because “the heart works harder” but because certain areas of the myocardium whose coronary vessels have lost the ability for compensatory dilatation are exposed to the biochemical hypoxiating influence of acute catecholamine discharges accompanying various stresses. Except in cases of far advanced coronary sclerosis, the term “coronary insufficiency” is to be understood as meaning inability of the coronary circulation to compensate by adequate dilatation for sympathogenic (catecholamine-induced) excessive myocardial oxygen losses.