EFFECT OF CAPTOPRIL TREATMENT ON TOTAL AND CENTRAL VASCULAR CAPACITANCE IN DOGS WITH CHRONIC HEART-FAILURE

Chronic rapid right ventricular pacing (RRVP) at 250 beats/min produce s low cardiac output (CO) heart failure, marked reduction in total vas cular capacitance, and a shift in volume centrally. The effect of conv erting enzyme inhibition with captopril on cardiac preload was investi gated in this model of heart failure. Eight splenectomized dogs were t reated with captopril (6.4 mg/kg daily) for 3 days before and 35 +/- 3 days (mean +/- SEM) after continuous RRVP was initiated and the outco me was compared with that of 5 untreated dogs subjected to RRVP for 32 +/- 3 days. Similar reductions in systemic arterial pressure (Psa) an d CO and increases in right atrial pressure (Pra) and total peripheral resistance (TPR) were noted in both groups, however, pulmonary capill ary 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 diffe rent blood volumes (TBV) during transitory cardiac arrests with acetyl choline (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 Pm cf 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 proportio n 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 associ ated with heart failure during RRVP.