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葡萄糖和哇巴因对去表皮和未去表皮金鱼肠道跨上皮电阻及细胞体积的影响。

Effects of glucose and ouabain on transepithelial electrical resistance and cell volume in stripped and unstripped goldfish intestine.

作者信息

Albus H, Groot J A, Siegenbeek van Heukelom J

出版信息

Pflugers Arch. 1979 Dec;383(1):55-66. doi: 10.1007/BF00584475.

Abstract
  1. In goldfish intestine (perfused unstripped segments and mucosal strips) the serosal addition of ouabain (10(-4) M) resulted in a vanishment of the transepithelial potential difference and in a continuous increase in transepithelial resistance. 2. Incubation of mucosal strips with ouabain resulted in an increase in sodium content which was greater than the decrease in potassium content. The resulting increase in cation content was accompanied by an increase in chloride content and an increase in water content. 3. Histological examination showed that exposure to ouabain resulted in a swelling of the epithelial layer as compared to the control situation. 4. The ouabain induced resistance increase is greater in the presence of glucose, 3-OMG or fructose than in the presence of mannitol. Phlorizin (10(-4) M) inhibits the extra resistance increase induced by mucosal glucose but is without effect on the fructose induced extra resistance increase. The initial velocity and the magnitude of the glucose induced extra resistance increase depends on the glucose concentration. 5. The results suggest that in goldfish intestine ouabain induces cellular swelling with a concomitant collapse of the lateral intercellular spaces, which is the cause of the increased transepithelial resistance. The additional changes in resistance induced by sugars suggest that the cell membrane is more permeable to glucose, 3-OMG and fructose than to mannitol. The resulting changes in osmotically active material within the epithelial cell influence the cross-sectional area and consequently the conductivity of the paracellular shunt pathway. The hypothesis that these sugars do not induce a resistance change in the absence of ouabain is discussed.
摘要
  1. 在金鱼肠道(未剥离的灌注段和黏膜条)中,向浆膜侧添加哇巴因(10⁻⁴ M)会导致跨上皮电位差消失,并使跨上皮电阻持续增加。2. 用哇巴因孵育黏膜条会导致钠含量增加,且增加幅度大于钾含量的减少幅度。阳离子含量的增加伴随着氯含量的增加和水含量的增加。3. 组织学检查表明,与对照情况相比,暴露于哇巴因会导致上皮层肿胀。4. 在存在葡萄糖、3 - O - 甲基葡萄糖或果糖的情况下,哇巴因诱导的电阻增加比在存在甘露醇的情况下更大。根皮苷(10⁻⁴ M)可抑制黏膜葡萄糖诱导的额外电阻增加,但对果糖诱导的额外电阻增加没有影响。葡萄糖诱导的额外电阻增加的初始速度和幅度取决于葡萄糖浓度。5. 结果表明,在金鱼肠道中,哇巴因诱导细胞肿胀,同时侧细胞间隙塌陷,这是跨上皮电阻增加的原因。糖诱导的电阻额外变化表明,细胞膜对葡萄糖、3 - O - 甲基葡萄糖和果糖的通透性比对甘露醇更高。上皮细胞内渗透活性物质的相应变化会影响横截面积,进而影响细胞旁分流途径的电导率。讨论了这些糖在不存在哇巴因时不会诱导电阻变化的假设。

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