Effect of Captopril Treatment on Total and Central Vascular Capacitance in Dogs with Chronic Heart Failure

SUMMARYChronic rapid right ventricular pacing (RRVP) at 250 beats/min produces low cardiac output (CO) heart failure, marked reduction in total vascular capacitance, and a shift in volume centrally. The effect of converting enzyme inhibition with captopril on cardiac preload was investigated in this model of heart failure. Eight splenec-tomized dogs were treated with captopril (6.4 mg/kg daily) for 3 days before and 35 ± 3 days (mean ± SEM) after continuous RRVP was initiated and the outcome was compared with that of 5 untreated dogs subjected to RRVP for 32 ± 3 days. Similar reductions in systemic arterial pressure (Psa) and CO and increases in right atrial pressure (Pra) and total peripheral resistance (TPR) were noted in both groups, however, pulmonary capillary wedge pressure (Ppcw) was higher in the untreated group (18.4 ± 1.6 vs. 12.1 ± 2.0 mm Hg). Total vascular compliance and capacitance was estimated from mean circulatory filling pressures (Pmcf) at different blood volumes (TBV) during transitory cardiac arrests with acetylcholine (ACh). Pmcf after chronic RRVP was higher in untreated animals (12.6 ± 1.9 vs. 8.4 ± 0.7 mm Hg) and compliance was lower (1.9 ± 0.2 vs. 2.6 ± 0.2 ml/mm Hg/kg). Total vascular capacitance at a Pmcf of 6 mm Hg was lower in untreated animals (50 ± 6 vs. 68 ± 3 ml/kg). Central vascular capacitance was also lower in untreated animals because Ppcw was higher and central blood volume (CBV) as a proportion of TBV was higher (21 ± 3 vs. 15 ± 2%). Four of 5 untreated and 1 of 8 treated dogs had severe ascites. Captopril treatment attenuated the marked reduction in total and central vascular capacitance associated with heart failure during RRVP.