原钒酸钠对小鼠肠运动的影响(英文)

来源 :哈尔滨医科大学学报 | 被引量 : 0次 | 上传用户:lcmeng
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目的探讨原钒酸钠对小鼠肠运动的影响及作用机制。方法采用碳末推进实验观察经胃给予小鼠原钒酸钠后胃肠推进率的变化,同时应用离体肠管观察原钒酸钠对小鼠十二指肠运动的影响,并同步测量药物对翻转小肠囊的葡萄糖-钠转运电位的影响。结果与正常组比较,不同剂量原钒酸钠均可提高小鼠胃肠推进率(P<0.05)。原钒酸钠浓度为10μmol/L,20μmol/L,30μmol/L时,十二指肠收缩张力分别为0.97±0.10,0.99±0.11,1.02±0.12,较对照组(0.87±0.11)高(P<0.05);收缩幅度分别为0.52±0.05,0.54±0.07,0.7±0.11,也高于对照组(0.50±0.05,P<0.05),但对收缩频率无明显影响(P>0.05)。此外,原钒酸钠浓度为10μmol/L和20μmol/L时,肠壁电势差(PD)分别为2.26mV±0.35mV,2.09mV±0.34mV,明显低于对照组(2.61mV±0.37mV,P<0.05)。结论原钒酸钠对离体和在体肠运动均有显著促进作用,这可能是通过抑制小肠葡萄糖-钠转运电位而发挥作用的。 Objective To investigate the effect and mechanism of sodium orthovanadate on intestinal motility in mice. Methods The effect of sodium orthovanadate on the gastrointestinal propulsive rate was observed by intragastric administration of sodium end-vanadate in mice. The effect of sodium orthovanadate on duodenal motility in mice was observed with the intestinal tract in vitro. Simultaneously, The effect of inverting the glucose-sodium transport potential of the small intestine sac. Results Compared with the normal group, different doses of sodium orthovanadate increased the rate of gastrointestinal propulsion in mice (P <0.05). Compared with the control group (0.87 ± 0.11), the contractile tension of duodenum was significantly higher than that of the control group (P <0.05) when the sodium orthovanadate concentration was 10μmol / L, 20μmol / L and 30μmol / <0.05). The amplitude of contraction was 0.52 ± 0.05, 0.54 ± 0.07 and 0.7 ± 0.11 respectively, which was also higher than that of the control group (0.50 ± 0.05, P <0.05), but had no significant effect on the contraction frequency (P> 0.05). In addition, the intestinal wall potential differences (PD) were 2.26mV ± 0.35mV and 2.09mV ± 0.34mV when the sodium orthovanadate concentration was 10μmol / L and 20μmol / L, respectively, which was significantly lower than that of the control group (2.61mV ± 0.37mV, P <0.05). Conclusion Sodium orthovanadate can significantly promote both in vitro and in vivo intestinal motility, which may play a role by inhibiting intestinal glucose-sodium transport potential.
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