卡托普利对尼古丁所致大鼠血管内皮功能损伤的保护作用

目的:探讨卡托普利对尼古丁损伤大鼠肠系膜动脉内皮依赖性舒张功能的保护作用及其机制。方法:将30只大鼠分为3组,即正常对照组、尼古丁损伤组(2mg·kg-1)、卡托普利组(尼古丁2mg·kg-1+卡托普利3mg·kg-1),4周后检测各组肠系膜动脉环血管舒张率及血清一氧化氮(NO)含量,一氧化氮合成酶(NOS)、超氧化物歧化酶(SOD)活性。结果:尼古丁使肠系膜动脉环血管舒张率明显降低,并伴随血清NO含量及NOS、SOD活性的明显下降(P<0.01或P<0.05);而卡托普利可升高血管舒张率,并且抑制了尼古丁诱导的NO含量及NOS、SOD活性的下降(P<0.01)。结论:卡托普利对尼古丁所致的血管内皮功能损伤具有明显保护作用,该作用可能与其抗氧化、促进内皮细胞合成、释放NO有关。

Protective Effect of Captopril on Nicotine-induced Endothelial Dysfunction in Rats

OBJECTIVE： To discuss the protective effect of captopril on the nicotine - induced impairment of endothelium- dependent relaxation （EDR） in rat mesenteric arteries and explore the possible mechanisms underlying the observed protective effects of captopril. METHODS： A total of 30 rats were randomly divided into 3 groups： normal control group, nicotine group （2 mg·kg^-1）, captopril group （nicotine 2 mg ·kg^-1＋ captopril 3 mg ·kg^-1）. After treatment for 4 weeks, vasodilatation rate of mesenteric arteries, the content of NO and NOS, and the SOD activities in serum were measured. RESULTS： Nicotine significantly decreased the vasodilatation rate of mesenteric arteries and decreased the content of NO and NOS, SOD activities in serum （P〈 0.01 or P〈 0.05）. However, captopril significantly increased the vasodilatation rate and inhibited the nicotine - induced decreases of the content of NO and the activities of NOS and SOD （P 〈 0.01） . CONCLUSION ： Captopril has remarkable protection on nicotine- induced endothelial dysfunction possibly related to its antioxidation, promoting synthesis of endothelial cells and NO release.