野百合碱诱导大鼠肺动脉高压及肺源性心脏病的病理生理特征

Pathophysiological charateristics of rat pulmonary hypertention and cor pulmonale induced by monocrotalire

目的:探讨野百合碱诱发肺动脉高压及肺源性心脏病模型的建立机制。方法:雄性Wistar大鼠20只,随机分为两组(n=10):正常组,模型组。模型组大鼠腹腔一次性注射野百合碱50 mg/kg,对照组注射同剂量的溶媒,28 d后测定大鼠血流动力学参数,硝酸盐还原酶法测定血清和肺组织中一氧化氮的含量;放射免疫法测定血浆中内皮素、脑钠素和肺组织中肿瘤坏死因子、内皮素的含量。结果:与对照组比较,右心室压力上升、心率和平均动脉压下降,血液和肺组织中肿瘤坏死因子、一氧化氮、内皮素-1、脑钠素含量上升,具有统计学意义。结论:野百合碱通过诱发肺血管和组织炎性损伤,升高体内肿瘤坏死因子、一氧化氮、内皮素-1的含量,建立肺动脉高压及肺源性心脏病模型。

Objective： To explore the mechanism of pulmonary hypertension and Cor Pulmonale rat models induced by monecrotaline （MCT）. Methods： Twenty 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 hemodynamie parameters were assessed; levels of tumour necrosis factor-α （TNF-α）, nitric oxide （NO）, endothelin-l（ET-1）,B-type natriuretic peptide（BNP） in pulmonary tissue or blood were measured using radio immunoassay or nitrate reduetase method. Results： 28 days af- ter MCT injection, compared with control group, fight ventricle systolic pressure （RVSP） increased and heart rate（HR）, mean arterial pres- sure （MAP） decreased; Levels of TNF-α, NO, ET-1 in pulmonary tissue or blood increased significantly in MCT group. Conclusion： The potential mechanism of MCT- induced pulmonary hypertension and Cor Pulmonale rat models associates with increasing TNF-α, NO, ET-1 levels in vivo, which results from inflammatory injury of lung tissue and blood vessels induced by MCT.