The effects of acute head injury or subarachnoid hemorrhage on the cardiovascular system (CVS) are well known, but data are lacking on the effects of acute spinal cord injury (SCI) on the CVS. The clip compression SCI rat model was used to measure changes in the mean systemic arterial pressure (mSAP), cardiac output (CO), heart rate (HR), total peripheral resistance (TPR), and central venous pressure (CVP) after SCI. Three groups of five animals each were anesthetized with chloralose-urethane: one group underwent only the surgical procedures including laminectomy, and the other two received either a 2.3- or 53.0-gm injury at the T1 spinal cord segment for 1 minute. The CO was measured using the thermodilution technique. CVS parameters were measured before injury, and then at designated times for 135 minutes after SCI. Analysis of variance and paired t-test with significance at p = 0.05 were used for analysis. There were no CVS changes as a result of anesthesia, operative time, or laminectomy alone. Cardiovascular system (CVS) changes occurred after the 2.3- and 53.0-gm. injuries but were significantly different only in the 53.0-gm injured animals. In this group mSAP increased from a preinjury value of 105 +/- 8 mm Hg to 178 +/- 11 mm Hg as a result of SCI, followed by a prolonged period of hypotension (46 +/- 15 mm Hg) lasting until 135 min post SCI. The CO after SCI also decreased from 394 +/- 22 to 218 +/- 29 ml/min/kg with the TPR reaching a minimal level at 45 min post SCI (265 +/- 23 to 213 +/- 29 mm Hg/ml/min gm wt), after which it returned to preinjury values. There were no significant changes in the CVP in either group. In the 53.0-gm group significant bradycardia (492 +/- 7 to 356 +/- 44 beats/min) was observed by 45 min and continued to decrease until 135 min after SCI. Thus the CVS showed two major alterations after severe SCI: post-traumatic hypotension, and a parallel decline in CO. There were no major changes in TPR, HR, or CVP, although HR ultimately declined. These findings suggest that the decline in CO was not entirely due to decreased sympathetic tone, but may also have resulted from direct myocardial injury, similar to that demonstrated after head injury or subarachnoid hemorrhage.