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哇巴因诱导金鱼肠黏膜跨上皮电阻增加的分析。

Analysis of the ouabain-induced increase in transepithelial electrical resistance in the goldfish intestinal mucosa.

作者信息

Groot J A, Albus H, Bakker R

出版信息

Pflugers Arch. 1981 Nov;392(1):67-71. doi: 10.1007/BF00584584.

Abstract
  1. The ouabain-induced increase in transmural resistance of goldfish intestinal mucosa stripped free from underlying muscular layers is analysed by comparing the resistance increase in normal and in low chloride saline, the resistance increased induced by anaerobic conditions and the resistance increase provoked by hypotonicity. 2. It is concluded that the collapse of the lateral intercellular space is the prime reason for the resistance increase and that the lateral intercellular space is maintained dilated by a ouabain-sensitive solute transport mechanism. 3. This mechanism can be either a rheogenic or a neutral Na/K-pump. In the latter case additional conditions have to be specified concerning values for ion concentrations in the lateral intercellular space and in the unstirred layer adjacent to the luminal membrane. 4. There are no indications for a chloride dependent mechanism involved in the maintenance of the width of the lateral intercellular spaces in the goldfish intestinal mucosa.
摘要
  1. 通过比较正常盐水和低氯盐水中的电阻增加、无氧条件诱导的电阻增加以及低渗性引发的电阻增加,分析了哇巴因诱导的从金鱼肠黏膜下层剥离的跨壁电阻增加情况。2. 得出结论:细胞间外侧间隙的塌陷是电阻增加的主要原因,且细胞间外侧间隙通过一种对哇巴因敏感的溶质转运机制保持扩张。3. 这种机制可以是生电的或中性的钠/钾泵。在后一种情况下,必须明确细胞间外侧间隙和靠近腔膜的未搅动层中离子浓度的附加条件。4. 没有迹象表明氯离子依赖性机制参与维持金鱼肠黏膜中细胞间外侧间隙的宽度。

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