摘要
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.
出处
《中国应用生理学杂志》
CAS
CSCD
2012年第3期193-196,I0001,共5页
Chinese Journal of Applied Physiology
基金
国家重大新药创制科技重大专项(2008ZX09101-006
2008ZXJ09004-018
2009ZX09301-002)