Transport functions of the gallbladder.

Transport functions of the gallbladder.
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胆囊的运输功能。

DOI:
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发表时间:
1980
期刊:
International review of physiology
影响因子:
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通讯作者:
K. Heintze
K. Heintze
中科院分区:
--
文献类型:
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作者:
Frizzell Ra;K. Heintze

文献摘要

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胆囊的吸收功能负责在进餐间歇期集中胆汁酸的Na+盐。这完全可以归因于其以等渗比例吸收氯化钠(和碳酸氢钠)和水的能力,从而使肝脏胆汁的体积减少了80%-90%。使用几个物种的胆囊的研究结果与中性氯化钠(和碳酸氢钠)吸收的存在是一致的,这是由于在粘膜存在耦合的(一对一)氯化钠进入过程。Na+从细胞内排出到浆膜液中,为细胞内的氯离子积聚提供能量,从而为跨上皮氯离子的转运提供能量。氯离子从细胞中渗出到浆膜溶液的机制尚不清楚,需要进一步研究。兔胆囊为研究氯化钠共转运提供了理想的准备,并将继续成为进一步研究这一机制的首选组织。电生理研究支持非导电氯化钠共转运的概念,并提出偏离严格中性盐吸收的过程可能与Na+和/或Cl-跨粘膜移动的额外(扩散)途径的存在有关,从而消除了这些离子吸收运动之间中性交配的机械约束。在此条件下,可观察到显著的浆膜阳性跨上皮PD,部分Cl-吸收可能与Na+电耦合。水通过渗透耦合到电解质运输而被被动地吸收。在细胞间隙的外侧水平,上皮内产生的高渗区为渗透水流动提供驱动力。鉴于胆囊的高渗透水渗透性,说明吸水率所需的高张程度可能比最初预期的要小,很可能很难在实验中检测到。最近对体液和药物对电解质和水运输的影响的研究表明,液体吸收的速度可能受到生理调节。例如,促胆汁分泌素可以刺激富含HCO3的胆汁分泌,也可以抑制胆囊重吸收富含HCO3的液体,这样可以加速十二指肠腔的中和。旨在确定胆囊吸收功能的生理控制的研究应该为未来的研究提供一个令人兴奋的途径。
The absorptive functions of the gallbladder are responsible for concentrating the Na+ salts of bile acids during interprandial periods. This can be attributed entirely to its ability to absorb NaCl (and NaHCO3) and water in isotonic proportions, thus reducing the volume of hepatic bile by 80%--90%. The results of studies employing gallbladders of several species are consistent with the presence of neutral NaCl (and NaHCO3) absorption that is due to the presence of a coupled (one-for-one) NaCl entry process at the mucosal membrane. Active Na+ extrusion from cell to serosal solution appears to provide the energy for cellular Cl- accumulation, and thus for transepithelial Cl- transport. The mechanism of Cl- exit from the cell to serosal solution is uncertain andrequires further study. Rabbit gallbladder provided an ideal preparation for the characterization of NaCl cotransport and continues to be the tissue of choice for further study of this mechanism. Electrophysiological studies support the concept of nonconductive NaCl cotransport and also suggest that departures from the process of strictly neutral salt absorption may be related to the presence of additional (diffusional) pathways for Na+ and/or Cl- movement across the mucosal membrane so that the mechanistic constraint of neutral copuling between the absorptive movements of these ions is removed. Under these conditions, a significant serosa-positive transepithelial PD is observed and a fraction of Cl- absorption may be electrically coupled to that of Na+. Water is absorbed passively by virtue of osmotic coupling to electrolyte transport. A region of hypertonicity generated within the epithelium, at the level of the lateral intercellular space, provides the driving force for osmotic water flow. In view of the high osmotic water permeability of the gallbladder, the degree of hypertonicity required to account for the rate of water absorption is probably smaller than originally anticipated and is likely to be difficult to detect experimentally. Recent studies of the effects of humoral and pharmacological agents on electrolyte and water transport suggest that the rate of fluid absorption may be subject to physiological regulation. For example, secretin, which stimulates a HCO3--rich biliary secretion, also inhibits the reabsorption of this HCO3--rich fluid by the gallbladder, and in this manner may expedite the neutralization of the duodenal lumen. Inquires aimed at defining the physiological control of the absorptive functions of the gallbladder should provide an exciting avenue for future studies.