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目的:探讨雷米普利酸(Ramiprilat)对内外源性自由基所致家兔离体胸主动脉内皮依赖性舒张功能损伤的保护作用及其作用机制。方法:采用DPPH(0.25μmol/L)或通过次黄嘌呤(HX 0.06μmol/L)和黄嘌呤氧化酶(XO 2U/L)孵育家兔离体血管环10 min,诱导血管内皮依赖性舒张功能损伤。结果:DPPH和HX+XO诱导产生氧自由基超氧阴离子(O-.2),能明显抑制胸主动脉环对乙酰胆碱(Ach)诱导的血管内皮依赖性舒张反应。用雷米普利酸(5μmol/L)预孵育血管环20 min,可明显改善DPPH和HX+XO所致血管内皮依赖性舒张反应的抑制。而预先用选择性缓激肽B2受体阻断剂HOE140(10μmol/L)孵育血管10 min,可明显抑制雷米普利酸对DPPH和HX+XO所致血管内皮依赖性舒张反应的损伤保护作用。结论:雷米普利酸对DPPH和HX+XO所致血管内皮依赖性舒张反应的损伤具有保护作用,其机制至少部分是通过激活缓激肽B2受体所介导的。
Objective: To investigate the protective effect and mechanism of Ramiprilat on endothelium-dependent vasodilatation injury induced by endogenous and exogenous free radicals in isolated thoracic aorta of rabbits. Methods: The isolated rabbit rings were incubated with DPPH (0.25μmol / L) or hypoxanthine (0.06μmol / L) and xanthine oxidase (XO2U / L) for 10 min to induce endothelium-dependent vasodilation damage. RESULTS: Oxygen free radical superoxide anion (O-2) was induced by DPPH and HX + XO, which markedly inhibited the acetylcholine-induced endothelium-dependent vasorelaxation of thoracic aorta rings. Pretreatment of vascular rings with ramipril acid (5 μmol / L) for 20 min significantly improved the inhibition of endothelium-dependent vasorelaxation induced by DPPH and HX + XO. Preincubation of vascular endothelial cells with selective bradykinin B2 receptor antagonist HOE140 (10μmol / L) for 10 min significantly inhibited the protective effect of ramipril against endothelium-dependent vasodilation induced by DPPH and HX + XO effect. CONCLUSION: Ramipril has a protective effect on the injury of endothelium-dependent vasorelaxation induced by DPPH and HX + XO, and its mechanism is at least partly mediated by the activation of bradykinin B2 receptor.