Graf J
Am J Physiol. 1983 Mar;244(3):G233-46. doi: 10.1152/ajpgi.1983.244.3.G233.
Studies on canalicular electrolyte transport are reviewed with reference to the concept that hepatocellular inorganic ion secretion may provide an osmotic drive for canalicular water flow. Cellular transport of electrolytes and of some nonelectrolytes appears directly or indirectly (cotransport or potential-sensitive transport) related to the activity of Na+-K+-ATPase of the sinusoidal cell membrane, but the role of the enzyme in regulating bile flow remains undetermined. Bile secretion of the isolated rat liver continues in the absence of either Na+, K+, Cl-, or HCO-3 when these ions are replaced in the perfusion medium by other permanent ions. Transepithelial salt concentration gradients, established experimentally, cause transient changes of bile flow and dissipate very quickly. Isotopic ion equilibration between sinusoids and bile proceeds faster than between sinusoids and liver cells. Both observations indicate extensive electrolyte diffusion through a paracellular shunt pathway. This pathway appears preferentially permeable to cations, and it restricts permeation of molecules of the size of sucrose (no apparent diffusion or effects of solvent drag) or bile acids (no backleak). In promoting canalicular osmotic water flow, transepithelial concentration gradients of NaCl are less effective than those of sucrose, revealing a reflection coefficient of NaCl of 0.3. By perfusion with hypertonic medium containing sucrose, bile flow is reduced. Bile production against this opposing osmotic gradient is accomplished by an increase in biliary organic anion concentration. Inorganic ion concentrations essentially conform to a Gibbs-Donnan distribution across the canalicular epithelium, established by the presence of impermeant anions in bile. Hence, the luminal electrical potential is expected to be negative with respect to the sinusoids. It is concluded that biliary secretion of endogenous organic anions is the major osmotic driving force for canalicular bile salt-independent bile flow and that transport of inorganic ions into bile results mainly from diffusion and solvent drag.
本文参考肝细胞无机离子分泌可能为胆小管水流提供渗透驱动力这一概念，对胆小管电解质转运的研究进行了综述。电解质和一些非电解质的细胞转运似乎直接或间接（协同转运或电位敏感转运）与肝血窦细胞膜上的Na⁺-K⁺-ATP酶的活性有关，但该酶在调节胆汁流动中的作用仍未确定。当灌注介质中的Na⁺、K⁺、Cl⁻或HCO₃⁻被其他永久性离子替代时，离体大鼠肝脏的胆汁分泌仍会继续。实验建立的跨上皮盐浓度梯度会导致胆汁流动的短暂变化，并很快消散。肝血窦与胆汁之间的同位素离子平衡比肝血窦与肝细胞之间的平衡进行得更快。这两个观察结果都表明电解质通过细胞旁分流途径进行广泛扩散。该途径似乎对阳离子优先通透，并且限制蔗糖（无明显扩散或溶剂拖曳效应）或胆汁酸（无回漏）大小的分子渗透。在促进胆小管渗透水流方面，NaCl的跨上皮浓度梯度比蔗糖的浓度梯度效果差，表明NaCl的反射系数为0.3。通过用含蔗糖的高渗介质灌注，胆汁流动减少。通过增加胆汁中有机阴离子浓度来克服这种相反的渗透梯度以产生胆汁。无机离子浓度基本上符合胆汁中存在不可渗透阴离子所建立的跨胆小管上皮的吉布斯-唐南分布。因此，预计管腔相对于肝血窦的电位为负。得出的结论是，内源性有机阴离子的胆汁分泌是胆小管胆汁盐非依赖性胆汁流动的主要渗透驱动力，并且无机离子向胆汁中的转运主要是由于扩散和溶剂拖曳。
