[Pathophysiological characteristics of rat pulmonary hypertension and cor pulmonale induced by monocrotaline].

OBJECTIVE: To explore the mechanism of pulmonary hypertension and Cor Pulmonale rat models induced by monocrotaline (MCT). METHODS: Twenty Wistar male rats were randomly divided into normal control group and model group (n= 10), which received a single intraperitoneal injection of MCT solution (50 mg/kg , the first day) or dissolvant, respectively. On day 28 after MCT administration, the hemodynamic parameters were assessed; levels of tumour necrosis factor-alpha (TNF-alpha), nitric oxide (NO), endothelin-1 (ET-1), B-type natriuretic peptide(BNP) in pulmonary tissue or blood were measured using radio immunoassay or nitrate reductase method. RESULTS: 28 days after MCT injection, compared with control group, right ventricle systolic pressure (RVSP) increased and heart rate(HR), mean arterial pressure (MAP) decreased; Levels of TNF-alpha, NO, ET-1 in pulmonary tissue or blood increased significantly in MCT group. CONCLUSION: The potential mechanism of MCI- induced pulmonary hypertension and Cor Pulmonale rat models associates with increasing TNF-alpha, NO, ET-1 levels in vivo, which results from inflammatory injury of lung tissue and blood vessels induced by MCT.