【摘要】 目的 :观察高静水压培养的人脐静脉内皮细胞 (HUVECs)内源性一氧化氮 (NO)合酶抑制物———不对称二甲精氨酸 (ADMA)的影响及卡托普利的保护作用。方法 :采用改良的Jaffe法培养原代HUVECs,取生长良好的3～ 6代HUVECs用于实验 ,分为①大气压组 :加等量DMEM培养液 ;②高静水压组 ;③高压加卡托普利组。测定上清液中ADMA、左旋精氨酸 (L arg)、NO和内皮素 (ET)的浓度 ,并测定血管紧张素转化酶 (ACE)的活性。结果 :高静水压组ADMA、ET的量、细胞内钙 [Ca2 + ]i及ACE活性增加 ,而NO的量减少。卡托普利干预后 ,上清液中ADMA、ET的浓度减少 ,ACE活性降低 ,NO的量增加 ,而L arg水平无明显变化。结论 :高静水压通过增加ADMA导致内皮功能紊乱 ,卡托普利则能通过减少ADMA减轻高压导致的内皮细胞代谢功能障碍更多还原

【Abstract】 Objective:To observe the effects of high hydrostatic pressure on metabolism of asymmetric NG, NG-dimethyl- L-arginine (ADMA)in human vascular endothelial cells(HUVECs)and the protection of captopril on it. Method: HUVECs of 3-6 th passage, cultured with modified Jaffes’ method, were enrolled into the experiment and divided into three groups: ①atmosphere (0 kPa, APC) group; ②high hydrostatic pressure ( 23.9 kPa, HPC) group; ③drug intervention groups. Concentrations of ADMA, L-arginine, nitric oxide(NO), endothim(ET), [Ca 2+]i and the activity of angiotensin-converting enzyme(ACE) in medium were measured. Result:Compared with APC, concentrations of ADMA, ET, [Ca 2+]i and the activity of ACE were increased, the amount of NO decreased. In the effect of captopril, ADMA, ET concentrations and the activity of ACE were decreased in a dose-dependent manner, while the level of L-arg had no obvious change. Conclusion:High hydrostatic pressure upregulates ADMA, while captopril may relieve endothelial dysfunction by decreasing ADMA concentration.更多还原