Sernka T J, Rood R P, Mah M Y, Tseng C H
Prostaglandins. 1982 Mar;23(3):411-26. doi: 10.1016/0090-6980(82)90086-7.
Ulcerative colitis is distinguished by abundant prostaglandin E2 (PGE 2) in the stools and by severe diarrhea. To determine whether luminal PGE2 alters normal colonic absorption, NA+ and Cl-transport across isolated rat proximal colon were studied before and after 16,16 dimethyl PGE2 (dmPGE2) addition to flux chambers. Luminal administration of dmPGE2 significantly reduced the net mucosal to serosal fluxes of Na+ and Cl-. These antiabsorptive tive effects of dmPGE2 on NA+ and Cl- active transport were reflected by a reduced metabolic rate of colonic tissue slices incubated with dmPGE2. Addition of dmPGE2 significantly reduces oxidation of glucose by the colon. Structurally, dmPGE2 reduced the length of colonic mucosal microvilli, thereby decreasing absorptive surface area. These results suggest that PGE2 released into the colonic lumen of patients with ulcerative colitis exerts antiabsorptive effects on the colon and in this way contributes to the associated diarrhea.
溃疡性结肠炎的特征是粪便中含有大量前列腺素E2（PGE2）以及严重腹泻。为了确定肠腔内的PGE2是否会改变正常的结肠吸收，在向通量室中添加16,16-二甲基PGE2（dmPGE2）之前和之后，研究了Na+和Cl-跨分离的大鼠近端结肠的转运情况。向肠腔给药dmPGE2显著降低了Na+和Cl-从黏膜到浆膜的净通量。dmPGE2对Na+和Cl-主动转运的这些抗吸收作用表现为与dmPGE2一起孵育的结肠组织切片代谢率降低。添加dmPGE2显著降低了结肠对葡萄糖的氧化。在结构上，dmPGE2缩短了结肠黏膜微绒毛的长度，从而减少了吸收表面积。这些结果表明，释放到溃疡性结肠炎患者结肠腔内的PGE2对结肠发挥抗吸收作用，进而导致相关腹泻。
