Whang E E, Dunn J C, Liu C D, Newton T, Zinner M J, McFadden D W, Ashley S W
Department of Surgery, UCLA School of Medicine, Los Angeles, California 90024, USA.
J Surg Res. 1996 Feb 1;60(2):303-6. doi: 10.1006/jsre.1996.0047.
Meal-stimulated colonic absorption has recently been described, but the cellular transport mechanisms mediating this response are unknown. The purpose of this study was to determine the contribution of Na+ transport pathways to colonic proabsorption. Distal colonic Thiry-Vella loops were constructed in six dogs. Absorption was measured by infusing the loops with a physiological electrolyte solution containing [14C] polyethylene glycol as the impermeant marker. In the first set of experiments, the dose dependence of amiloride-induced inhibition of basal colonic absorption was determined. In the second set of experiments the effect of amiloride, which inhibits both Na+ channels and Na+/H+ exchange in colonocytes, on meal-stimulated colonic absorption was determined. Luminal amiloride inhibited basal colonic absorption in a dose-dependent manner, with significant reductions in Na+ absorption occurring with concentrations of 10(-2)M and higher. Infusion with 10(-3)M amiloride, a concentration that did not alter basal absorption, resulted in significant reductions in postprandial water, Na+, and Cl- absorption. These results suggest that meal-stimulated colonic absorption is mediated, at last in part, by transcellular Na+ absorptive pathways.
近期已有关于进餐刺激后结肠吸收的报道，但介导这种反应的细胞转运机制尚不清楚。本研究的目的是确定Na⁺转运途径对结肠促吸收作用的贡献。在6只犬身上构建了远端结肠的Thiry-Vella肠袢。通过向肠袢中输注含有[¹⁴C]聚乙二醇作为非通透标记物的生理电解质溶液来测量吸收情况。在第一组实验中，确定了氨氯地平诱导的基础结肠吸收抑制的剂量依赖性。在第二组实验中，确定了抑制结肠细胞中Na⁺通道和Na⁺/H⁺交换的氨氯地平对进餐刺激的结肠吸收的影响。管腔内氨氯地平以剂量依赖性方式抑制基础结肠吸收，浓度为10⁻²M及更高时Na⁺吸收显著降低。输注10⁻³M氨氯地平（该浓度不改变基础吸收）导致餐后水、Na⁺和Cl⁻吸收显著降低。这些结果表明，进餐刺激的结肠吸收至少部分是由跨细胞Na⁺吸收途径介导的。
