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目的观察阿托伐他汀对野百合碱(monocrotaline,MCT)诱导的大鼠肺动脉压及肺部炎症的影响。方法将24只SD大鼠随机分为正常对照组(对照组),MCT诱导的肺动脉高压组(PH模型组),阿托伐他汀干预组(治疗组),每组8只。PH模型组和治疗组分别一次性腹部皮下注射MCT(60mg/kg),治疗组自注射MCT之日起以阿托伐他汀(10mg/kg)灌胃,每日1次。3周后达实验终点,测定大鼠平均肺动脉压、计算右心室肥大指数。肺组织切片进行HE染色,取肺组织观察肺小动脉周围炎症细胞浸润程度,并计算肺中、小动脉管壁厚度占血管外径的百分比(WT%)和肺动脉管壁面积/管总面积的百分比(WA%),以此反映肺血管重建情况。结果治疗组大鼠的平均肺动脉压、右心室肥大指数、肺中、小动脉WT%和WA%均较PH模型组明显减小,血管周围炎明显减轻(P均﹤0.01)。大鼠肺组织炎性细胞计数与平均肺动脉压、肺中、小动脉WT%和WA%均呈明显正相关(P均﹤0.01)。结论阿托伐他汀具有抑制MCT诱导的肺部炎症、肺血管重建和肺动脉高压形成的作用。
Objective To observe the effect of atorvastatin on pulmonary arterial pressure and pulmonary inflammation induced by monocrotaline (MCT) in rats. Methods Twenty-four Sprague-Dawley rats were randomly divided into normal control group, MCT-induced pulmonary hypertension group (PH model group) and atorvastatin intervention group (treatment group), with 8 rats in each group. The PH model group and the treatment group were given a single subcutaneous injection of MCT (60mg / kg) into the abdomen, and the treatment group was orally administered with atorvastatin (10mg / kg) once daily from the day of MCT injection. After 3 weeks, the experimental endpoint was reached. The mean pulmonary arterial pressure was measured and the right ventricular hypertrophy index was calculated. The lung tissue sections were stained with HE, the infiltration of inflammatory cells around the small pulmonary arteries was observed and the percentage of vascular wall thickness to the external diameter of the vessels (WT%) and the area of pulmonary artery wall / total area Percentage (WA%), reflecting pulmonary revascularization. Results The mean pulmonary arterial pressure, right ventricular hypertrophy index, WT% and WA% of the pulmonary arteries and small arteries in the treatment group were significantly decreased compared with those in the PH model group, and the perivascular inflammation was significantly reduced (all P <0.01). Inflammatory cell counts in lung tissue of rats were positively correlated with mean pulmonary arterial pressure, WT% and WA% of pulmonary artery and small artery (P <0.01). Conclusions Atorvastatin can inhibit MCT-induced pulmonary inflammation, pulmonary vascular remodeling and pulmonary hypertension.