二甲基氨氯吡咪对油酸诱导的血管内皮损伤的影响  

Protective Effect of Dimethyl Amiloride against Vascular Endothelium Injury Induced by Oleic acide

作　　者：张维文[1] 张贵平[1] 区慧坚[1] 

机构地区：[1]广州医学院药理教研室,广州510182

出　　处：《广州医学院学报》2001年第4期14-16,共3页Academic Journal of Guangzhou Medical College

摘　　要：目的:探讨钠氢交换抑制剂二甲基氨氯吡咪(ＤＭＡ)对低浓度油酸(ＯＡ)所致的血管内皮损伤的保护作用。方法:分别用ＯＡ及ＯＡ＋ＤＭＡ温育离体大鼠胸主动脉环,观察其对乙酰胆碱(Ａｃｈ),硝普钠(ＳＮＰ),Ｌ－Ｎ－硝基精氨酸甲酯(Ｌ－ＮＡＭＥ)的反应。结果:ＯＡ(１０－４ｍｏｌ·Ｌ－１)温育３０ｍｉｎ后,Ａｃｈ诱导的舒张反应减弱,最大舒张从６４%降低到２８%;Ｌ－ＮＡＭＥ诱导的收缩反应也减弱,最大收缩由５２%降低到３４%。而对ＳＮＰ诱导的舒张反应无影响。如用ＤＭＡ(１０－６ｍｏｌ·Ｌ－１)＋ＯＡ温育３０ｍｉｎ,则可部分恢复单用ＯＡ引起的Ａｃｈ的舒张反应及Ｌ－ＮＡＭＥ收缩反应的减弱,Ａｃｈ的最大舒张恢复到４７%,Ｌ－ＮＡＭＥ的最大收缩恢复到４５%。 结论:ＤＭＡ对ＯＡ所致的血管内皮损伤具有保护作用。ve:To study the protective effect of sodium-hydrogen exchanger inhibitor (NHEI) dimethyl amiloride ( DMA) against vascular endothelial injury induced by oleic acid ( OA). Methods; The responses of the isolated thoracic aortic rings of rats to acetylcholine ( Ach) , sodium nitroprusside (SNP) and NG-nitro-L-arginine methyl ester (L-NAME) were observed after the incubation with OA and OA + DMA respectively. Results; It was shown that after the incubation with OA ( 10-4mol · L-1) for 30 min, the vasorelaxation induced by Ach and the contraction induced by L-NAME were reduced, as compared with the control. The maximal vasorelaxation was reduced from 64% to 28% , and the maximal contraction from 52% to 34% . Incubation with DMA (10-6 mol ·L-1) + OA for 30 min partly reversed the effects of Ach and L-NAME, with the maximal vasorelaxation of 47% and maximal contraction of 45% . Conclusion: DMA can protect the vascular endothelium from damage induced by OA.

关 键 词：二甲基氨氯吡咪 钠氢交换抑制剂 油酸 血管内皮 

分 类 号：R963[医药卫生—微生物与生化药学]