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Stimulation by sparkling water of gastroduodenal HCO3- secretion in rats

机译:苏打水刺激大鼠胃十二指肠HCO3-的分泌

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Background We examined the effect of sparkling water on gastroduodenal HCO3- secretion in rats and investigated the factors involved in these responses. Material and Method Under urethane anesthesia, a chambered stomach or a proximal duodenal loop was superfused with saline, and HCO3- secretion was measured at pH 7.0 using a pH-stat. Results The amount of CO2 in sparkling water was about 7.2 g/L. The mucosal exposure with sparkling water increased the secretion of HCO3- in both the stomach and duodenum. The HCO3- response in the duodenum was partially inhibited by indomethacin, acetazolamide or sensory deafferentation and was totally abolished by the co-administration of the former two agents. By contrast, the response in the stomach was almost totally inhibited by acetazolamide and partially mitigated by indomethacin but not sensory deafferentation. DIDS [an inhibitor of the Cl-/HCO3- exchanger (AE) and the Na+-HCO3- cotransporter (NBC)] and DMA [an inhibitor of the Na+/H+ exchanger 1 (NHE1)] partially mitigated the HCO3- response in the duodenum but not the stomach. The mucosal application of sparkling water increased prostaglandin E2 content in these tissues. Conclusions Sparkling water stimulates HCO3- secretion in both the stomach and the duodenum, but the mechanisms involved differ in these two tissues; the response in the former is mainly due to the intracellular supply of HCO3- with the aid of carbonic anhydrase, while in the latter the response is dependent on the NHE1, AE and NBC, and is mediated by endogenous prostaglandins as well as capsaicin-sensitive afferent neurons, in addition to the intracellular supply of HCO3-.
机译:背景我们检查了苏打水对大鼠胃十二指肠HCO3-分泌的影响,并研究了参与这些反应的因素。材料和方法在氨基甲酸乙酯麻醉下,用生理盐水灌注有胃腔或十二指肠近端loop,并使用pH调节剂在pH 7.0下测量HCO3-的分泌。结果苏打水中的二氧化碳含量约为7.2 g / L。苏打水与粘膜接触增加了胃和十二指肠中HCO3-的分泌。吲哚美辛,乙酰唑胺或感觉性脱除咖啡因能部分抑制十二指肠中的HCO3-响应,而前两种药物的共同给药则完全消除了HCO3-响应。相比之下,乙酰唑胺几乎完全抑制了胃中的反应,吲哚美辛部分缓解了胃中的反应,但感觉上的脱除咖啡因反应没有。 DIDS [Cl- / HCO3-交换剂(AE)和Na + -HCO3-协同转运蛋白(NBC)的抑制剂]和DMA [Na + / H +交换剂1(NHE1)的抑制剂]部分缓解了HCO3-反应。十二指肠而不是胃。苏打水的粘膜应用增加了这些组织中前列腺素E2的含量。结论苏打水刺激胃和十二指肠中HCO3-的分泌,但是在这两个组织中所涉及的机制不同。前者的反应主要是由于碳酸酐酶在细胞内供应HCO3-,而后者的反应取决于NHE1,AE和NBC,并由内源性前列腺素和辣椒素敏感介导。传入神经元,除了细胞内供应的HCO3-。

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