摘要
目的研究TNF-α在缺氧性肺动脉高压中的作用。方法将32只SD大鼠分为:①正常组8只,不缺氧处理;②单纯缺氧组,每只于缺氧前腹腔注射生理盐水lml,每天缺氧8小时,共2周;③缺氧2周+TNF-α组:每天缺氧前腹腔注射TNF-α(0.26mg/kg);④缺氧2周+TNF-α+L-Arg组:每天缺氧前腹腔注射TNF-α(0.26mg/kg)和L-Arg(100mg/kg)。缺氧完成后测各组大鼠血流动力学改变,并作肺病理切片、肺血管图像分析。结果单纯缺氧组和加入TNF-α组其肺动脉压明显高于正常组和加入TNF-α+L-Arg组(2.98±0.34kPa和3.68±0.45kPaVS2.05±0.13kPa和2.35±0.19kPa),且各组间均有显著差异(P<0.05),单纯缺氧组和加入TNF-α组其肺小血管壁厚度和管壁面积均明显增加,显著高于正常组和加入TNF-α+L-Arg组,差异有显著性意义(P<0.05),单纯缺氧组和加入TNF-α组之间差异无显著性意义。结论TNF-α能增强慢性缺氧性肺动脉高压,L-Arg能拮抗其作用。
Objective To study the effects of TNF-αon the chronic hypoxic pulmonary hypertention in rats.Methods The animal model of chronic hypoxic pulmonary hypertention in rats were builted.At the same time,bolus injection of TNF-α(0.26mg/kg)and L-Arg(100mg/kg) were given in rats,then the hymodynamic and pathologic changes were observed.Results The mPAP which injected TNF-αgroup was significantly hight than the control group and hypoxic two weeks group(3.68±0.45kPa VS 2.05±0.13kPa and 2.98±0.34kPa,P<0.05). Comination injection TNF-αand L-Arg could decrease mPAP(2.35±0.19kPa).Hypoxic and TNF-αcould increase the pulmonary arteries's medial thickness and medial area.Conclusion TNF-αcan increase the hypoxic pulmonary hypertention and thicken the pulmonary arteries. L-Arg can antagonite the effects of TNF-α.
出处
《中国现代医药杂志》
2004年第5期24-26,共3页
Modern Medicine Journal of China
