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二氧化硫衍生物舒张大鼠离体主动脉血管环的效应及其机制研究 预览 被引量:22

Vasorelaxant effect of sulfur dioxide derivatives on isolated aortic rings of rats and its mechanisms
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摘要 目的:探讨二氧化硫(sulfur dioxide,SO2)及其衍生物的舒张血管作用及其机制。方法:离体大鼠主动脉环灌流,应用去甲肾上腺素(noradrenaline,NE)预收缩主动脉环后,观察其对SO2供体——亚硫酸钠/亚硫酸氢钠混合液(Na2SO3/NaHSO3,3:1物质的量比)的舒张反应;观察应用KATP通道阻断剂格列本脲和钙通道阻断剂尼卡地平对Na2SO3/NaHSO3血管效应的影响;观察应用内源性SO2生成酶抑制剂天冬氨酸异羟肟酸(hydroxamate,HDX)和Na2SO3/NaHSO3预孵育血管组织后NE缩血管效应的变化。结果:大鼠离体主动脉环对Na2SO3/NaHSO3呈浓度(0~12mmol/L)依赖性的舒张反应,IC50值为(7.28±0.12)mmol/L,最大舒张率(Emax)为78.79%±3.24%。格列本脲(1×10μmol/L)抑制低浓度Na2SO3/NaHSO3(≤4mmol/L)的舒血管效应,而对高浓度(〉6mmol/L)的舒血管效应无明显影响。经尼卡地平(1×10^-9mol/L)预孵育的血管环对NE的收缩反应明显减弱,Na2SO3/NaHSO3则不能舒张该血管。反之,预先用HDX(1×10^-4mol/L)孵育阻断内源性SO2生成后,血管环对NE的收缩反应增强[EC50从(6.48±0,84)×10^-7mol/L降至(3.97±1.63)×10^-7mol/L,P〈0.01];而用Na2SO3/NaHSO3预先孵育的血管对NE的收缩反应曲线右移[EC50从(6.48±0.84)×10^-7mol/L升至(4.93±0.81)×10^-5mol/L,P〈0.01]。结论:SO2具有明显的舒张血管平滑肌作用,其作用机制与钙离子通道及KATP通道有关,推测机体内源性SO2具有血管功能调节意义。 Objective : To investigate the vasorelaxant effect of sulfur dioxide ( SO2 ) on isolated aortic rings of rats in vitro and its relaxation mechanisms. Methods: We perffused the isolated aortic rings of rats, and precontracted the rings with noradrenaline (NE) , then observed the relaxant reactivity of SO2 derivatives, mixture of sulfite and hydrogen sulfite [ NaESO3/NaHSO3 3:1 (amount of substance)], to the aortic rings. Meanwhile, we studied the influence of glibenclamide and nicardipine, blockers of KATe and L-calcium channels, on the vasorelaxant reactivity of SO2 derivatives. We further incubated the aortic rings with hydroxamate (HDX) , the inhibitor of SO2 endogenous generating enzymes, and SO2 derivatives (4 mmol/L) in vitro, then observed the contraction of the aortic rings to NE. Results: Isolated aortic rings of rats exhibited relaxant reactivity to NaESO3/NaHSO3 (0 - 12 mmol/L) in a concentration-dependent manner. IC50 of the relaxation curve was (7.28 ±0.12 ) mmol/L, and Emax was 78.79% ± 3.24%. Glibenclamide (1×10^-6 mol/L) inhibited the vasorelaxation to low dose Na2SO3/NaHSO3 (≤4 mmol/L ), whereas it failed to inhibit the vasorelaxafion to high dose of NaESO3/NaHSO3 ( 〉 6 mmol/L). Nicardipine (1×10^-9 moL/L) could decrease the contraction of the rings to NE, and even could inhibit the relaxation of NaESO3/NaHSO3 almost completely. The inhibition of the endogenous SO2 production with HDX ( 1×10 ^-4mol/L) , resulted in an increase in the contraction of rings. The contraction curve to NE shifted to the left, and IC50 also changed from (6.48±0.84) × 10^-7mot/L to (3.97±1.63 )×10^-7 mol / L ( P 〈 0.01 ) . However, after the incubation of aortic rings with Na2SO3 / NaHSO3(4mmol/L), the contraction curve to NE shifted to the right, and IC50 changed from (6.48±0.84)×10^-7 mol/L to (4.93±0.81 )×10-^5mol/L (P 〈0.01 ). Conclusion: SO2 could relax vascular smooth muscles, and the mechanism might be associa
作者 杜淑旭 张春雨 金红芳 杜军保 唐朝枢 DU Shu-xu, ZHANG Chun-yu, JIN Hong-fang, DU Jun-bao, TANG Chao-shu(1. Department of Pediatrics, Peking University First Hospital, Beijing 100034, China; 2. Institute of Cardiovascular Diseases, Peking University First Hospital; 3. Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education)
出处 《北京大学学报:医学版》 CAS CSCD 北大核心 2006年第6期 581-585,共5页 Journal of Peking University:Health Sciences
基金 国家自然科学基金(30630031)及国家重点基础研究发展规划项目基金(2006CB503807)资助.
关键词 二氧化硫 血管舒张 平滑 血管 大鼠 Sulfur dioxide Vasodilation Muscle, smooth, vasular Rats
作者简介 Corresponding author's e-mail.junbaodu@ht.rol.cn.net
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