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Vasodilator effect of gaseous sulfur dioxide and regulation of its level by Acli in rat vascular tissues

机译:气态二氧化硫的血管舒张作用及Acli调节其在大鼠血管组织中的水平

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摘要

To explore the toxicological and physiological role of gaseous SO_2 on vascular contractility and its level in vascular tissues, a vasodilation study of isolated rat thoracic aortic rings by gaseous SO_2 was carried out. The level of SO_2 in vascular tissue was assayed using a modified high-performance liquid chromatographic method with fluorescence detection (HPLC-FD). The results show that gaseous SO_2 (from 1 muW to 2000 muM) relaxed rat thoracic aortic rings in a dose-dependent manner. The physiological concentrations of SO_2 in thoracic aortic tissues and plasma in rats were 127.76±31.34 muM and 16.77±8.24 muW, respectively; The vasorelaxant effect of gaseous SO_2 at physiological and low concentrations (<450 uM) was endothelium dependent, and at high concentrations (>500 muW) was endothelium independent. The results also show that SO_2 could be endogenously generated in vascular tissues, and mainly in vascular endothelial cells; acetylcholine (Ach) increased the SO_2 level in vascular tissue, and no adrenaline (NE) decreased the SO_2 level. These findings demonstrate that gaseous SO_2 is a vasorelaxant substance, and the vasorelaxant effect of gaseous SO_2 is much stronger than that of its derivatives sulfite and bisulfite, which result from the inactivation process of SO_2 gas transmitter by which SO_2 is hydrated to form sulfite, and the latter is enzymatically oxidized to form sulfate.These findings also demonstrate that endogenous SO_2 level in vascular tissue may be regulated by Ach and NE.
机译:为了探讨气态SO_2对血管收缩性及其在血管组织中的水平的毒理和生理作用,进行了气态SO_2对离体大鼠胸主动脉环血管扩张的研究。采用改良的高效液相色谱-荧光检测法(HPLC-FD)测定血管组织中的SO_2水平。结果表明,气态SO_2(从1μW到2000μM)以剂量依赖的方式使大鼠胸主动脉环松弛。大鼠胸主动脉组织和血浆中SO_2的生理浓度分别为127.76±31.34μM和16.77±8.24μW。气态SO_2在生理和低浓度(<450 uM)时的血管舒张作用与内皮有关,而在高浓度(> 500μW)时与内皮无关。结果还表明,SO_2可以在血管组织中内源性产生,主要在血管内皮细胞中产生。乙酰胆碱(Ach)增加了血管组织中SO_2的水平,而没有肾上腺素(NE)降低了SO_2的水平。这些发现表明,气态SO_2是一种血管舒张物质,而气态SO_2的血管舒张作用远强于其衍生物亚硫酸盐和亚硫酸氢盐,这是由于SO_2气体传输剂的失活过程导致的,SO_2被水合形成亚硫酸盐,并且这些发现还表明,血管组织中的内源性SO_2水平可能受Ach和NE的调节。

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