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Objective : ⑴. Establish a practical , can be better simulated clinical cases of the pathogenesis of pulmonary hypertension in rats animal models ; ⑵. Role of hepatocyte growth factor in the pathogenesis of pulmonary hypertension process in the animal model and its possible mechanisms. Methods : SD rats underwent left lung resection 1 week subcutaneous injection of monocrotaline alkali ( MCT 60mg/kg ) ; control group underwent a sham surgery , pulmonary artery pressure measurement , one week after subcutaneous injection of saline . Experimental animals 1, 2, 3, 4 weeks after the MCT injection manometry again , then sacrificed , specimens from the right lung , heart and other samples for pathology detection and molecular analysis , in order to understand the pulmonary vascular remodeling and HGF / c-met, eNOS, TGF-β and ET-1 cytokine expression in the lung tissue volume changes. Results: Compared with the control group , 28 days after MCT injection in rats with severe signs of right heart failure , were significantly increased mean pulmonary artery pressure , right ventricular hypertrophy degrees ; microscope, obviously pulmonary vascular remodeling , and for the right lung fibrosis , pulmonary artery endothelial and medial smooth muscle layer hyperplasia , vascular density ; lung tissue of HGF eNOS expression was significantly reduced , TGF-β and ET-1 was significantly higher ( P lt; 0.01 ) , and c-met remained not change (P gt; 0.05), changes in expression levels of these cytokines and pulmonary vascular remodeling , there is a clear correlation . Conclusion : ⑴ method left lobe resection surgery composite subcutaneous injection of monocrotaline pulmonary hypertension in animal models to establish a novel , indeed , provide a reliable experimental basis for the further study of pulmonary hypertension ; ⑵. Lungs of rats HGF expression down may be the main reason for pulmonary hypertension in this animal model ; , eNOS expression lowered due to the production of NO reduction and the increase of ET-1 is the main reason for the high pulmonary artery pressure . ⑶ lungs of TGF-β expression was significantly higher may be of HGF synthesis reduce important reason .
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