Class Trypsin, Chymase, Macrophage Inflammatory Factor 1¦Á, Oxidative Damage In The Mechanism Of Pulmonary Hypertension And The Role Of Simvastatin Statin Intervention

Objective:we establish a SD rat model of pulmonary hypertension induced by high pulmonary blood flow associated with monocrotaline administration to investigate the change of the mast cell in the pulmonary hypertension after simvastatin treatment.Methods:an arterial-venous shunt was surgically created between the abdominal aorta and inferior vena cava in rats except the control group. Simvastatin(2mg/kg) was administered 2 days after the operation . Monocrotaline (60mg/kg) was administered 7 days after the creation of the aorto-caval fistula. 35 days after the operation, mean pulmonary artery pressure(mPAP) of all rats were measured by cardiac catheterization.The animals'hearts were isolated to calculate the ratio of right ventricle mass to left ventricle plus septum mass (RV/LV+S).Immunohistochemical stains were used to show the tryptase+ mast cell and the chymase+ mast cell distribution in order to observe the change of the mast cell in the model group , the control group and the treatment group. Using HE stain to observe the pathological change in lung.Results: HE stain indicates the obvious thicken of the artery, RV/ (LV+S ) and mPAP elevated obviously (P<0.05) in model group in comparison with the control group, they were also elevated obviously (p<0.05) in the model group compared with the treatment group. The tryptase+ mast cell and the...