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孟紫强, 张海飞. 二氧化硫衍生物对大鼠离体主动脉环收缩影响[J]. 中国公共卫生, 2005, 21(12): 1412-1414. DOI: 10.11847/zgggws2005-21-12-03
引用本文: 孟紫强, 张海飞. 二氧化硫衍生物对大鼠离体主动脉环收缩影响[J]. 中国公共卫生, 2005, 21(12): 1412-1414. DOI: 10.11847/zgggws2005-21-12-03
MENG Ziqiang, ZHANG Haifei. Effect of SO2 derivatives on isolated thoracic aorta rings in rats[J]. Chinese Journal of Public Health, 2005, 21(12): 1412-1414. DOI: 10.11847/zgggws2005-21-12-03
Citation: MENG Ziqiang, ZHANG Haifei. Effect of SO2 derivatives on isolated thoracic aorta rings in rats[J]. Chinese Journal of Public Health, 2005, 21(12): 1412-1414. DOI: 10.11847/zgggws2005-21-12-03

二氧化硫衍生物对大鼠离体主动脉环收缩影响

Effect of SO2 derivatives on isolated thoracic aorta rings in rats

  • 摘要:
      目的   研究二氧化硫衍生物对大鼠离体胸主动脉的舒张作用及其可能的作用机制。
      方法   将离体大鼠胸主动脉环固定于营养液浴槽中, 给药后记录血管环张力变化。
      结果   二氧化硫衍生物对有无内皮的血管均有舒张作用。二氧化硫衍生物对去甲肾上腺素(NE)、氯化钾(KCl)和钙离子(Ca2+)引起的血管收缩呈非竞争性拮抗作用, 其拮抗系数分别为0.43, 2.03, 2.49。在无钙液中NE引起的细胞内外钙流增加可被二氧化硫衍生物抑制。作用与同条件下的维拉帕米相似。
      结论   二氧化硫衍生物的舒张作用与内皮无关, 能抑制电压依赖性钙通道和受体依赖性钙通道, 并能抑制内钙的释放。对此尚需进一步研究证实。

     

    Abstract:
      Objective   To investigate the relaxant effect and its mechanism of SO2 derivatives(sulfite and bisulfite, 3:1 mol/L)on the isolated thoracic aorta rings in rats.
      Methods   Isolated rat aortic mucle rings were used to perfuse in chambers containing chemicals tested in Kerbs buffer and the ring tensions were recorded.
      Results   SO2 derivatives had relaxant effects on thoracic aorta with and without endothelium.The contraction responses induced by norepinephrine(NE), potassium chloride(KCl), and Ca2+ were antagonized SO2 derivatives in a non-competitive manner.The pD' 2 values were 0.43, 2.03, 2.49 respectively.In Ca2+-free modified Krebs solution, the contraction of two components induced by NE were inhibited significantly by SO2 derivatives.The effect features of SO2 derivatives mentioned above were just like that of verapamil in the same experimental conditions.
      Conclusion   The relaxant effect of SO2 derivatives on rat's thoracic aorta is not dependent on endothelium, and is closely related to the blockage of Ca2+ entry through both potential-deqendent calcium channel and receptor-operating calcium channel, and to the inhibition of intracellular Ca2+ release.

     

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