Cardiovascular Effects of 1,1,1-Trichloroethane

Abstract

Acute exposure of anesthetized dogs to 1,1,1-trichlorothane (TCE) results in a dose-dependent, biphasic decline in arterial pressure similar to that observed following exposure to a commercial solvent containing TCE. The initial phase of pressure decline is associated with peripheral vasodilation whose magnitude exceeds concomitant, reflex, positive chronotropic and inotropic effects on myocardial function. The peripheral dilation could be reversed by injection of the α-agonist, phenylephrine hydrochloride. The second phase of pressure decline is primarily associated with a depression of myocardial function; heart rate, stroke output, and myocardial contractility declined. Injection of Ca⁺⁺ ameliorated the TCE-induced alteration of myocardial contractility and blood pressure was protected. The data suggest that comprehension of the mech- anism(s) by which TCE induces cardiovascular depression may lead to more effective clinical management of the toxic effects of this compound.