VASCULAR CAPACITANCE AND CARDIAC-OUTPUT IN PACING-INDUCED CANINE MODELS OF ACUTE AND CHRONIC HEART-FAILURE

The relationship between stressed and total blood volume, total vascul ar capacitance, central blood volume, cardiac output (GO), and pulmona ry capillary wedge pressure (Ppcw) was investigated in pacing-induced acute and chronic heart failure. Acute heart failure was induced in an esthetized splenectomized dogs by a volume load (20 mL/kg over 10 min) during rapid right ventricular pacing at 250 beats/min (RRVP) for 60 min. Chronic heart failure was induced by continuous RRVP for 2-6 week s (average 24 +/- 2 days). Total vascular compliance and capacitance w ere calculated from the mean circulatory filling pressure (Pmcf) durin g transient circulatory arrest after acetylcholine at three different circulating volumes. Stressed blood volume was calculated as a product of compliance and Pmcf, with the total blood volume measured by a dye dilution. Central blood volume (CBV) and CO were measured by thermodi lution. Central (heart and lung) vascular capacitance was estimated fr om the plot of Ppcw against CBV. Acute volume loading without RRVP inc reased capacitance and CO, whereas after volume loading with RRVP, cap acitance and CO were unaltered from baseline. Chronic RRVP reduced cap acitance and CO. All interventions, volume +/- RRVP or chronic RRVP, i ncreased stressed and central blood volumes and Ppcw. Acute or chronic RRVP reduced central vascular capacitance. Cardiac output was increas ed when stressed and unstressed blood volumes increased proportionatel y as during volume loading alone. When CO was reduced and Ppcw increas ed, as during chronic RRVP or acute RRVP plus a volume load, stressed blood volume was increased and unstressed blood volume was decreased. Thus, interventions that reduced CO and increased Ppcw also increased stressed and reduced unstressed blood volume and total vascular capaci tance.