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中文摘要：
探讨二氧化硫（SO2）及其衍生物（Na2SO3／NaHSO3）引起大鼠血管舒张作用与细胞信号转导的关系．采用放射免疫分析技术测定不同浓度SO2衍生物染毒组和正常组大鼠胸主动脉血管环中环磷酸腺苷（cAMP）、环磷酸鸟苷（cGMP）及前列环素（PGI2）和血栓素（TXA2）的代谢产物6-酮-前列腺素F1α（6-Keto—PGF1α）和血栓素B2（TXB2）的浓度，以及腺苷酸环化酶（AC）活性．结果表明：①在离体大鼠胸主动脉血管中，cAMP和6-Keto—PGF1α的含量随二氧化硫衍生物浓度的增高而显著升高，且呈一定的剂量效应关系；②AC活性也随SO2衍生物浓度的增高而增高；③而cGMP的含量在SO2衍生物各浓度组均略微降低，但只有4mmol／L组降低显著；cAMP／cGMP比值在各浓度组与正常对照组（CK）相比均有显著性升高；④TXB2的含量在各浓度组均无明显变化；但6-Keto／TXB2比值显著升高．试验得出，SO2衍生物作用于血管组织产生PGI2，后者通过激活AC使胞内cAMP增高，即通过PGI2-AC-cAMP信号转导途径引起血管舒张，血压下降．表2参13
英文摘要：
To study cell signal transduction pathway on vasodilatation rats caused by sulfur dioxide derivatives, levels of cAMP, cGMP, 6-Keto-PGF1α, TXB2 and activity of adenylyl cyclase in the isolated aortic rings of rats were determined by radioimmunoassay. The results indicated that SO2 derivatives could greatly increase the levels of cAMP and 6-Keto-PGF1α in the isolated rat aortic rings in a dose-dependent manner; SO2 derivatives also caused large increase in adenylyl cyclase activity in a dose-dependent manner; cGMP level was decreased, cAMP/cGMP ratios were significantly increased at all SO2 groups; no change in TXB2 was observed at all SO2concentrations tested. However, 6-Keto/TXB2 was significantly increased by exposure to SO2derivatives at 2 mmol/L and 4 mmol/L. It was demonstrated that SO2 derivatives caused an increase in PGI2, then AC was activated by PGI2 and AC enhanced the production of cAMP, later caused vasodilatation of blood vessel of rats. Tab 2, Ref 13
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