摘要
目的 :旨在研究ET 1对大鼠肺和全身脂质过氧化损伤作用 ,以明确ET 1致大鼠ALI的作用机制。方法 :2 8只健康雄性Wistar大鼠 ,随机分为两组 :内皮素组经股静脉持续滴注ET 1,对照组用生理盐水代替。检测两组动物实验前后呼吸频率、血气分析、支气管肺泡灌洗液 (BALF)中蛋白含量、白细胞及分类计数、肺系数、肺组织学检查以及肺实质、BALF、全血中脂质过氧化物 (LPO)、超氧化物歧化酶 (SOD)、谷胱甘肽 (GSH)的含量。结果 :ET 1诱导出大鼠ALI ,内皮素组较对照组肺实质、BALF中LPO含量升高 ,SOD含量下降 (P <0 .0 1) ,全血LPO含量升高 ,SOD含量下降 (P<0 .0 5 ) ,BALF中GSH含量下降 (P <0 .0 1)。结论 :ET 1能够引起大鼠肺部脂质过氧化损伤效应。ET 1可能是机体内源性的致肺损伤因子之一。
Objective: To clarify the role of ET-1 in rats with acute lung injury (ALI) through investigating the effect of ET-1 on lipid peroxidation injury to the lung and the general body of the rats. Methods: 28 male wister rats were randomly divided into two groups. ET-1 were continuously injected through the femoral vein in experimental group while normal saline was used in control group instead. The respiratory rate, arterial blood gas, the levels of protein in bronchoalveolar lavage fluid (BALF), the white blood cell count and differential count of BALF, lung coefficient, lung histological changes were observed, and the levels of lipid peroxide (LPO),superoxide dismutase (SOD), glutathione (GSH) in the lung homogenate,BALF,and whole blood were measured. Results: ET-1 can induce ALI in rats. The endothelin group has a significant increase in LPO and decrease in SOD in the lung homogenate and BALF comparing to that of control group ( P < 0.01), as well as whole blood ( P < 0.05), the level of GSH in BALF were significantly decreased ( P < 0.01). Conclusion: ET-1 can induce lung tissue damages due to its injurious effect of causing lipid peroxidation and ET-1 may be one of the endogeneous ALI-inducing factors.
出处
《内科急危重症杂志》
2002年第3期129-131,136,共4页
Journal of Critical Care In Internal Medicine
