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

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。

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

Objective: To explore the mechanism of pulmonary hypertension and Cor Pulmonale rat models induced by monocrotaline(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 hemodynamic parameters were assessed;levels of tumour necrosis factor-α(TNF-α),nitric oxide(NO),endothelin-1(ET-1),B-type natriuretic peptide(BNP) in pulmonary tissue or blood were measured using radio immunoassay or nitrate reductase method.Results: 28 days after MCT injection,compared with control group,right ventricle systolic pressure(RVSP) increased and heart rate(HR),mean arterial pressure(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.