Hemodynamics in dogs with pulmonary hypertension due to emphysema

We examined hemodynamic parameters in a canine model of pulmonary emphysema in which the lesion was severe enough to increase transmural mean pulmonary artery pressure ( {Mathematical expression}) to about 10 mmHg higher than a control group of dogs. Pulmonary emphysema was produced in 6 dogs (Group E) by the repeated weekly instillations of the enzyme papain administered into their lobar bronchi. In 5 control dogs (Group C), a normal saline solution was used. Pulmonary hemodynamics and gas exchange measurements were obtained after 7 doses of the enzyme were administered when, relative to the prepapain value, total lung capacity had increased by 40% in Group E. Hemodynamic measurements were performed before and after plasma volume expansion to elevate the mean transmural wedge pressure ( {Mathematical expression}) to approximately 15 mmHg. At similar cardiac outputs and {Mathematical expression}, {Mathematical expression} in Group E were higher than in Group C in both the pre (mean ±SD; 7.3 ± 1.4 mmHg vs 18.5 ± 5.5 mmHg, P < 0.01) and volume-loaded (21.7 ± 2.2 vs 27.9 ± 4.7 mmHg, P < 0.01) conditions. Compared with Group C, arterial blood oxygen tension and diffusing capacity for carbon monoxide were reduced in Group E. Left ventricular performance was normal in Group E, whereas right ventricular performance appeared slightly depressed. The latter finding was explained in terms of a relatively increased right ventricular afterload in Group E, which impeded right ventricular ejection.