OBJECTIVETo explore the mechanism of pulmonary hypertension and Cor Pulmonale rat models induced by monocrotaline (MCT).

METHODSTwenty 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.

RESULTS28 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.

CONCLUSIONThe 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.

Animals ; Disease Models, Animal ; Endothelin-1 ; metabolism ; Hypertension, Pulmonary ; chemically induced ; metabolism ; physiopathology ; Lung ; metabolism ; Male ; Monocrotaline ; adverse effects ; Nitric Oxide ; metabolism ; Pulmonary Heart Disease ; chemically induced ; metabolism ; physiopathology ; Rats ; Rats, Wistar ; Tumor Necrosis Factor-alpha ; metabolism