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为了探索二氧化硫(SO2)作为调节血管张力的细胞气体信号分子的可能性,采用SO2衍生物(亚硫酸钠和亚硫酸氢钠混合物,在中性液体中二者的摩尔比约为3:1)温育大鼠离体胸主动脉血管环的方法,观察SO2及其衍生物对血管环张力的影响.结果发现,SO2及其衍生物在低浓度(<1.35mmol·L-1)下可引起大鼠离体胸主动脉血管环收缩而不引起舒张;在高浓度(>1.35mmol·L-1)下先引起血管环收缩、后引起舒张;且这些变化均与血管内皮无关.这表明不同作用浓度相和不同作用时相,该化学物对血管张力的作用完全相反.由此得出结论:1)低浓度SO2及其衍生物是血管收缩因子;2)高浓度SO2及其衍生物对血管张力的影响是双相-双向性的.内源性的SO2及其衍生物的前体SO/SO2在体内的生理浓度比本研究的低浓度还要低1～2个数量级,其对血管张力的生理作用及其他的生物学作用尚需进一步研究.
To explore the potential of sulfur dioxide (SO2) as a cellular gas signaling molecule that regulates vascular tone, SO2 derivatives (a mixture of sodium sulfite and sodium bisulfite in a molar ratio of about 3: 1 in a neutral liquid) were incubated Rat thoracic aortic vascular ring method to observe the SO2 and its derivatives on the vascular ring tension.It was found that SO2 and its derivatives at low concentrations (<1.35mmol·L-1) can cause rats In vitro, the vasoconstriction of the thoracic aorta was not caused by diastole, and the vasoconstriction was induced at high concentration (> 1.35mmol·L-1), then the vasodilatation was induced. All of these changes were independent of the vascular endothelium, indicating that different concentrations Phase and different phases of action, the effect of this chemical on vascular tension is exactly the opposite, which leads to the conclusion: 1) low concentrations of SO2 and its derivatives are vasoconstriction factors; 2) the effect of high concentrations of SO2 and its derivatives on vascular tone Is bi-phasic-bi-directional.The endogenous SO2 and its precursors SO2 and SO2 precursors in the body physiological concentration than the low concentration of this study even lower 1 to 2 orders of magnitude, the vascular tension Physiological effects and other biological effects need further study.