Effects of E. coli endotoxemia on ventricular performance

Publisher Website
Google Scholar
Abstract
The extent to which the development of shock associated with E. coli endotoxemia is consequent to depression of myocardial contractility has not heretofore been systematically examined. Left ventricular function was studied in cats, utilizing a preparation designed to permit control of systemic arterial pressure, cardiac output, heart rate, and temperature. Data were obtained permitting the inscription of ventricular function curves, relating stroke volume and mean ejection rate to ventricular end-diastolic pressure (LVEDP) at constant heart rate and aortic pressure (100 mm Hg). Within 15-30 min of the administration of E. coli endotoxin (Difco), 5 mg/kg, the contractility of the left ventricle was reduced, as evidenced by a sharp reduction in the stroke volume and mean ejection rate for a given LVEDP. The continuous administration of angiotensin II, 1-2.5 [mu]g/kg per min, following endotoxemia often resulted in a substantial improvement in left ventricular function, whereas prior to endotoxemia an inotropic effect could rarely be elicited. Equal amounts of isoproterenol resulted in a substantially greater positive inotropic response in the endotoxin-depressed heart. It is concluded that E. coli endotoxemia in the cat reduces the contractility of the left ventricle. It is suggested that this mechanism may contribute importantly to circulatory failure in endotoxin shock.