内源性气态SO_2对血管的舒张作用及其机制Ⅱ:与亚硫酸盐的比较及SO_2的内源产生与调节The Vasorelaxant Effect of Endogenous Gaseous Sulfur Dioxide on Aortic Rings and Its Mechanism Ⅱ:A Comparison with Sulfite Effects and SO_2 Biosynthesis and Regulation
孟紫强;李君灵;张全喜;白维铭;杨振华;王法琦;赵颖;
摘要(Abstract):
为了探讨内源性气态SO2对血管的舒张作用及其机制,采用将气态SO2或SO2生理盐水溶液加入孵育液,使SO2分子直接作用于离体大鼠胸主动脉血管环的方法,对体内SO2的失活机制、正常生理浓度及其内源产生的体内调节等进行了研究,并对亚硫酸盐/亚硫酸氢盐能否作为"SO2供体"的问题进行了讨论.结果显示:1)气态SO(21~2000μmol·L-1)对血管的舒张作用是剂量依赖性的,且其舒血管作用远大于SO2衍生物(亚硫酸盐和亚硫酸氢盐),表明SO2衍生物是SO2信号作用失活的产物;2)SO2气体和SO2生理盐水溶液对大鼠血管的舒张作用强度相似,表明在SO2生理学或毒理学试验中二者可相互替代;3)正常大鼠胸主动脉血管组织和血浆中内源性SO2平均浓度分别为(127.76±31.34)和(16.77±8.24)μmol·L-1,表明血管组织SO2的浓度很高;4)内源性SO2在血管内皮和平滑肌细胞均可合成,但主要在血管内皮细胞合成;5)不论对大鼠体内血管组织还是对离体血管组织、体外培养的血管内皮和平滑肌细胞,乙酰胆碱(Ach)均能剂量依赖性地促进SO2的产生,而重酒石酸去甲肾上腺素(NE)能够抑制SO2产生.由此结论:1)SO2生理作用的失活途径为"气态SO2→亚硫酸盐/亚硫酸氢盐→硫酸盐",亚硫酸盐和亚硫酸氢盐混合液的作用并不能等同于内源性SO2的作用,不能作为体内、外处理生物组织的"SO2供体";2)直接应用SO2气体或者应用SO2生理盐水溶液代替SO2气体处理生物组织可作为内源性SO2生理学研究的新模式;3)血管组织SO2的浓度很高且主要在内皮细胞合成;4)SO2的生物合成也能被体内某些内源性物质(如Ach、NE)所调节.
关键词(KeyWords): 二氧化硫;二氧化硫衍生物;亚硫酸盐;生理浓度;调节;气体信号分子;血管舒张作用;SO2供体
基金项目(Foundation): 国家自然科学基金项目(No.20677035;No.20477023);; 山西省自然科学基金项目(No.20031092)
作者(Author): 孟紫强;李君灵;张全喜;白维铭;杨振华;王法琦;赵颖;
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