Epidemiologic studies provided evidence that increased heart disease mortality after carbon disulfide exposure is not only related to carbon disulfide-caused coronary sclerosis but they suggest that there would be reversible, direct cardiotoxic effects. In order to investigate such direct toxic effects of carbon disulfide on the cardiovascular system, in this study carbon disulfide was administered acutely and subacutely to rats. Blood pressure and heart rate in normotensive conscious unrestrained rats were not markedly influenced by both acute and subacute carbon disulfide administration. Depressant effects of carbon disulfide administration on intracardiac impulse generation and conduction as well as on contractile force were observed in urethane-anesthetized rats. The appearance of several forms of aconitine-induced arrhythmias was delayed after subacute treatment with carbon disulfide. In the coronary occlusion model, subacute carbon disulfide treatment reduced the survival rate accompanied by marked influences on arrhythmia development. Our results show that short term carbon disulfide exposure alters cardiac function in rats under physiological and pathophysiological conditions.