An Experimental Animal Model of Postobstructive Pulmonary Hypertension

Background

A small experimental animal model of postobstructive pulmonary hypertension (PH) providing insights in the physiopathology of this disease was developed.

Materials and methods

Male Lewis rats were anesthetized and aleatory manipulated via a left thoracotomy with (group I, n = 10) or without (group II, n = 10) ligation of the left pulmonary artery. Animals were followed for 2 weeks and then sacrificed. Hemodynamic parameters and blood gases were recorded at baseline and 2 weeks after surgical procedure.

Results

Group I animals developed a significant (P < 0.01) PH (mean pulmonary artery pressure, 32 ± 6 versus 16 ± 2 mm Hg; pulmonary vascular resistance, 46 ± 3 versus 21 ± 2 mm Hg/mL/min; reduction of cardiac output, 75 ± 3 versus 105 ± 4 mL/min), compared to group II animals, and had a significant (P < 0.01) worse gas exchange (partial arterial pressure of O₂: 91 ± 3 versus 439 ± 24 mm Hg; partial arterial pressure of CO₂: 54 ± 3 versus 42 ± 2 mm Hg, on a fraction of inspired oxygen of 1.0), right ventricle hypertrophy (ventricle to left ventricle/septum ratio, 0.56 ± 0.04 versus 0.45 ± 0.04, P < 0.02) and less tolerance test (immobility time, 123 ± 11 versus 61 ± 8 s, P < 0.01) than group II animals. Histologically, ligated lungs showed postobstructive pulmonary vasculopathic abnormalities and bronchial-pulmonary artery hypertrophy, and the contralateral lung had initial signs of small vessel arteriopathy.

Conclusions

The experimental model generated here successfully reproduced a PH morphologically and functionally similar to clinical postembolic PH and might be used for evaluating the physiopathology of postobstructive PH.

Key Words: chronic pulmonary hypertension, lung embolism, pulmonary artery ligation, right ventricle hypertrophy