肺动脉高压大鼠T型和TC型肥大细胞的改变

Change of MCT and MCTC in Pulmonary Hypertension

目的:建立SD大鼠高肺血流并用野百合碱注射所致肺动脉高压模型,观察肺组织中肥大细胞及肥大细胞两种亚型的变化,探讨肥大细胞在肺动脉高压中的机制。方法:大鼠腹主动脉-下腔静脉造瘘,术后7天一次性腹腔注射野百合碱60mg/kg,制造肺动脉高压模型,35天后测定肺动脉压,取肺组织进行免疫组织化学染色,观察肥大细胞的变化,HE染色观察肺组织一般病理变化。结果:HE染色显示肺组织中动脉管壁明显增粗,有新生血管形成。平均肺动脉压力模型组较对照组升高(P<0.05);右心室/(左心室+室间隔)模型组较对照组增加(P<0.05),肥大细胞总数及类糜蛋白酶阳性的肥大细胞模型组较对照组增多(P<0.05)。结论:腹主动脉-下腔静脉造瘘合并野百合碱腹腔注射成功的建立了肺动脉高压的动物模型,肥大细胞在肺组织的聚集以及活化、肥大细胞亚型的改变可能是肺动脉高压形成的机制之一。

Objective:SD rat model of pulmonary hypertension was established by high pulmonary blood flow associated with monocrotaline administration to observe the change of the mast cell in the pulmonary hypertension.Method:An arterial-venous shunt was surgically created between the abdominal aorta and inferior vena cava in rats except the control group.Monocrotaline (60 mg/kg) was administered 7 days after the creation of the aorto-caval fistula. 35 days after the operation,mPAP were measured by cardiac catheterization. Immunohistochemical stains were used to show the tryptase+ mast cell and the chymase+ mast cell distribution.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 (P<0.05) in model group in comparision with the control group. The tryptase+ mast cell and the chymase+ mast cell increased in the model group compared with the control group.Conclusion: Aorto-caval fistula plus monocrotaline administration successfully established a rat model of pulmonary hypertension. The accumulation and activation of mast cell and the change of the subtype may be one of the mechanism of the pulmonary hypertension.