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Title: Original rat model of high kinetic unilateral pulmonary hypertension surgically induced by combined surgery. Author: Meng L, Liu X, Zheng Z, Li J, Meng J, Wei Y, Hu S. Journal: J Thorac Cardiovasc Surg; 2013 Nov; 146(5):1220-1226.e1. PubMed ID: 23395098. Abstract: OBJECTIVES: The characteristic morphologic lesions observed in the lungs of patients with congenital cardiac anomalies have not been closely modeled in rat shunt-related models, except for the reversible grade 1 changes. The present study reported an original rat model of unilateral pulmonary hypertension surgically induced by combined surgery to reproduce more advanced pulmonary vascular lesions. METHODS: The right pulmonary artery was ligated through a right posterolateral thoracotomy, and a cervical shunt was established 1 week later. The immediate and chronic effects on the pulmonary hemodynamics were evaluated through right heart catheterization immediately after and at 8 and 12 weeks postoperatively. The morphologic changes in pulmonary vasculature were analyzed after staining with hematoxylin-eosin and modified Weigert's method. The right ventricular hypertrophy index was calculated and artery blood gas analysis performed. RESULTS: A pulmonary hypertensive status was successfully induced immediately after cervical surgery and progressively aggravated into a borderline state with disease course advancing. Pulmonary vasculopathy demonstrated a transition from reversibility (muscularization, intimal proliferation of grade 1-2) at 8 weeks to irreversibility (intimal fibrosis, entirely luminal occlusion, grade 3) at 12 weeks postoperatively. Conspicuous right ventricular hypertrophy and decreasing partial arterial pressure of oxygen were also observed. CONCLUSIONS: The present shunt-related model successfully simulated a hypertensive status in pulmonary circulation and reproduced the characteristic transition of pulmonary vasculopathy from reversibility to irreversibility within a relatively short period. Thus, this model could offer an alternative with low mortality and high reproducibility for investigations on the underling mechanisms of shunt-related pulmonary hypertension.[Abstract] [Full Text] [Related] [New Search]