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The purpose of this study was to investigate the hemodynamic responses, mainly cardiac output and regional blood flow, to converting enzyme inhibition by captopril in the intact and nephrectomized rabbit. Twenty-one New Zealand white rabbits anesthetized with pentobarbital had systemic arterial blood pressures measured and cardiac output and regional blood flow determined by the microsphere method. Captopril (1–3 mg/kg) significantly reduced cardiac output in the intact but not in nephrectomized rabbits. In both the intact and nephrectomized animals, captopril was associated with small but not significant decreases in blood pressure and no significant change in total peripheral vascular resistance or heart rate. Regional blood flow was reduced, but the fractional distribution of cardiac output to the myocardial, lung (bronchial), hepatic, and splanchnic (small intestine) circulations was unchanged after captopril. These data suggest that the reduction in cardiac output induced by converting enzyme inhibition may be attributed to a fall in venous return that in turn may be dependent on renal factors.

To determine whether arrhythmias persist in the chronic stage of myocarditis, serial electrocardiograms were studied in DBA/2 mice with experimentally induced myocarditis. After baseline electrocardiograms with standard limb and two precordial leads were recorded, 52 mice were inoculated intraperitoneally with 0.1 ml of the myocardiotropic variant of encephalomyocarditis in a viral suspension containing 102TCD50(50% tissue culture infective dose). Electrocardiograms were recorded every day on days 3 to 18 and, thereafter, once every 10 to 20 days until day 220. The cumulative incidence rate of myocarditis was 90.4% (47 of 52). No arrhythmias were found on baseline electrocardiograms. Serial electrocardiograms showed atrial and ventricular premature complexes and complete atrioventricular (AV) block, respectively, in 6 (12.8%), 8 (17.0%) and 25 (53.2%) of 47 mice with myocarditis. Myocardial lesions were found in the heart of mice with these ectopic complexes. Mononuclear cell infiltrations into the His bundle were noted in the conduction system of mice with complete AV block. Heart rate began to increase after day 11 (638 ± 105 beats/min, n = 16 versus control rate 557 ± 57 beats/min, n = 47, mean ± standard deviation, p < 0.01) and reached a maximum on day 15 (40 ± 22 beats/min, n = 8, p < 0.01). The sum of QRS voltage in eight leads began to decrease after day 6 (62.1 ± 18.8 mm, n = 24 versus control value 80.0 ± 14.7 mm, n = 47, p < 0.01) and reached a minimum on day 13 (32.5 ± 7.5 mm, n = 8, p < 0.01) when myocardial necrosis and congestion of the lungs and liver were most prominent. Thereafter, heart rate began to decrease and the sum of QRS voltage in eight leads to increase with time. On day 120, heart rate was 624 ± 24 beats/min and the sum of QRS voltage in eight leads was 67.1 ± 8.6 mm (n = 5). On days 16 to 220, atrial premature complexes or ventricular premature complexes, or both, remained in five (62.5%) of eight mice with myocarditis.