This study was designed to determine whether subchronic CO exposure ranging from 15 to 530 ppm induced modifications in the rat cardiovascular system. We investigated the degree of resistance to an in vitro transient ischemia in the hearts exposed in vivo to different CO concentrations for 1-4 weeks. Subchronic CO exposure induced dose and/or time-dependent increases (hematocrit, cardiomegaly and coronary flow). We showed an increase in the ventricular tachycardia (VT) incidence with the passing weeks of exposure, which demonstrated the proarrhythmic activity of CO even in low doses (15 ppm). The contractile recovery decreased owing to a low (50 ppm) or high (530ppm) CO exposure after a 25-min ischemia period. This diminution seems to be dependent on the increased amplitude of ischemic contracture. The present study supports the hypothesis that subchronic CO exposure, even at low levels of CO, can produce cardiovascular changes and could explain the increased risk of myocardial infarction.