Cardiovascular effects of acute normovolemic hemodilution in rats with disopyramide-induced myocardial depression.

The effect of myocardial depression on the circulatory response to acute normovolemic hemodilution (hematocrit 23%) with hetastarch was evaluated in 28 anesthetized Sprague-Dawley rats. Cardiac output was recorded using an electromagnetic flow probe. Mild, moderate, and severe myocardial depression were achieved by infusing disopyramide 50, 75, and 85 mg/kg. This resulted in a dose-dependent decrease in cardiac output (r = -0.73, p less than 0.05) and mean arterial pressure (r = -0.65, p less than 0.05), and an increase in left ventricular end-diastolic pressure (r = 0.77, p less than 0.05) and total peripheral resistance (r = 0.46, p less than 0.05). Following hemodilution, cardiac output and mean arterial pressure were significantly lower and total peripheral resistance significantly higher in animals with myocardial depression compared with saline anemic controls. These differences were dose-dependent for cardiac output (r = -0.83, p less than 0.05), mean arterial pressure (r = -0.68, p less than 0.05), and total peripheral resistance (r = 0.51, p less than 0.05). Although control animals were able to significantly increase their cardiac output and stroke volume after hemodilution compared with baseline, animals with severe myocardial depression were unable to do so. This resulted in marked hypotension after hemodilution in controls compared with severely depressed animals. The results suggest a diminished ability of the pharmacologically depressed heart to tolerate acute normovolemic hemodilution.