Hansen C P, Holstein-Rathlou N H, Skøtt O, Leyssac P P, Frederiksen O
Institute of Experimental Medicine, Panum Institute, University of Copenhagen, Denmark.
Acta Physiol Scand. 1991 Feb;141(2):185-95. doi: 10.1111/j.1748-1716.1991.tb09067.x.
Lithium (Li+) absorption across the low-resistance epithelium of the rabbit gall-bladder was studied in order to elucidate possible routes and mechanisms of Li+ transfer. Li+ at a concentration of 0.4 mM in both mucosal and serosal media did not affect isosmotic mucosa-to-serosa fluid absorption. At this low concentration net mucosa-to-serosa Li+ absorption was insignificant when the ambient Na+ concentration was 115 mM, although the gall-bladder had a significant Li+ permeability (2.7 X 10(-5) cm s-1) and a significant mucosa-to-serosa Li+ gradient developed as a result of fluid absorption. Net Li+ absorption was induced at reduced mucosal Na+ concentrations (by lowering the Na+ concentration down to 50 mM with or without substitution with sucrose, or by adding sucrose to the mucosal medium). This Li+ absorption occurred even in the absence of a mucosa-to-serosa Li+ gradient. Na+ and Li+ absorptions occurring at 50 mM Na+ were inhibited to the same degree by mucosal 1 mM amiloride. Substitution of 5-50 mM (44%) Na+ by Li+ in the external medium dose-dependently depressed Na+ absorption by up to 76%, while substitution by 50 mM choline had no significant effect. Li+ inhibition of Na+ absorption was elicited from the mucosal side and was not accounted for by compensatory Li+ absorption; water and Na+ absorption rates decreased nearly in parallel. The effects of 0.4 mM amiloride and of substitution with 20 mM Li+ were only partly additive. It is concluded that Li+ absorption in the rabbit gall-bladder cannot be explained by passive (paracellular) transport, but must be the result of transcellular, active transport. Both at low and at high concentrations Li+ may enter the cell via an Na+/H+ exchanger in the apical cell membrane. At high concentrations Li+ may inhibit Na+ absorption by interference with the exchange mechanism and/or via effects at the cytoplasmic level. The Li+ transfer mechanism across the basolateral cell membrane remains unknown.
为了阐明锂离子（Li+）转运的可能途径和机制，对兔胆囊低电阻上皮细胞对Li+的吸收进行了研究。黏膜和浆膜介质中Li+浓度均为0.4 mM时，不影响等渗的黏膜到浆膜的液体吸收。在此低浓度下，当环境Na+浓度为115 mM时，净黏膜到浆膜的Li+吸收不显著，尽管胆囊具有显著的Li+通透性（2.7×10−5 cm s−1），并且由于液体吸收形成了显著的黏膜到浆膜的Li+梯度。在降低的黏膜Na+浓度下（通过将Na+浓度降低至50 mM，无论是否用蔗糖替代，或通过向黏膜介质中添加蔗糖）诱导净Li+吸收。即使在不存在黏膜到浆膜的Li+梯度的情况下，这种Li+吸收也会发生。在50 mM Na+时发生的Na+和Li+吸收被黏膜中1 mM氨氯吡脒以相同程度抑制。在外部介质中用Li+替代5 - 50 mM（44%）的Na+剂量依赖性地使Na+吸收降低高达76%，而用50 mM胆碱替代则无显著影响。Li+对Na+吸收的抑制作用从黏膜侧引发，且不能用代偿性Li+吸收来解释；水和Na+的吸收速率几乎平行下降。0.4 mM氨氯吡脒和用20 mM Li+替代的作用仅部分相加。结论是，兔胆囊中的Li+吸收不能用被动（细胞旁）转运来解释，而必定是跨细胞主动转运的结果。在低浓度和高浓度下，Li+都可能通过顶端细胞膜中的Na+/H+交换体进入细胞。在高浓度下，Li+可能通过干扰交换机制和/或通过在细胞质水平的作用来抑制Na+吸收。跨基底外侧细胞膜的Li+转运机制仍然未知。
