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 O(2): 91 +/- 3 versus 439 +/- 24 mm Hg; partial arterial pressure of CO(2): 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.
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 O(2): 91 +/- 3 versus 439 +/- 24 mm Hg; partial arterial pressure of CO(2): 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.
Authors: Abraham Rothman; Robert G Wiencek; Stephanie Davidson; William N Evans; Humberto Restrepo; Valeri Sarukhanov; Amanda Rivera-Begeman; David Mann Journal: Comp Med Date: 2011-06 Impact factor: 0.982
Authors: Abraham Rothman; Robert G Wiencek; Stephanie Davidson; William N Evans; Humberto Restrepo; Valeri Sarukhanov; David Mann Journal: Pulm Circ Date: 2017-02-01 Impact factor: 3.017