卡托普利对大鼠血管内皮功能损伤的保护作用

Protective Effect of Captopril on Endothelial Dysfunction in Rat

目的探讨卡托普利对烟碱所致大鼠血管内皮功能损伤的影响及可能机制。方法将30只大鼠分为3组,即正常对照组、烟碱损伤组(2mg/kg,腹腔注射)、卡托普利保护组(烟碱2mg/kg,腹腔注射+卡托普利3mg/kg,静脉注射),4周后检测各组肠系膜动脉环内皮依赖性舒张(EDR)反应及主动脉一氧化氮(NO)含量,一氧化氮合成酶(NOS)和超氧化物歧化酶(SOD)活性变化。结果烟碱损伤组肠系膜动脉环EDR明显降低,并伴随主动脉NO含量及NOS,SOD活性的下降;卡托普利保护组血管EDR得到了明显改善,并且抑制了烟碱诱导的主动脉NO含量及NOS,SOD活性的下降。结论卡托普利对烟碱所致血管内皮功能损伤有明显保护作用,该作用与其清除氧自由基、促进内皮细胞合成、释放NO有关。

Objective To study the effects of captopril on nicotine- induced endothelial dysfunction in rats and to explore the possible mechanisms. Methods 30 rats were randomly divided into 3 groups： control group,nicotine group （2 mg/kg, i.p. ）,captopril group （nicotine 2 mg/kg,i.p. ＋captopril 3 mg/kg,i. v. ）. After 4 weeks,isometric tension recordings were used to assess EDR responses of mesenteric arteries. The content of NO and NOS ,SOD activities in aorta homogenates were measured. Results Administration of nicotine significantly impaired EDR responses compared with control group. This impairment was accompanied by a reduction in NO contents and NOS, SOD activities in aorta homogenates. However, chronic captopril treatment not only improved the impairment of EDR,but also prevented the reduction of NO contents and of NOS and SOD activities in the aorta. Conclusion This beneficial effect of captopril on nicotine- induced endothelial dysfunction is achieved not only by scavenging oxygen- free radicals,but also by preventing a reduction in NOS activity,thus enhancing NO production in endothelial cells.