Kocoshis S A, Wong C T
Department of Pediatrics, University of Pittsburgh School of Medicine, PA.
Ann Clin Lab Sci. 1991 May-Jun;21(3):197-204.
Previous studies by us suggested that luminally administered sodium salicylate blocks dihydroxy-bile acid-induced colonic secretion in the rat. In the present study, an in vivo rat cecal loop technique is employed to compare the effects of luminally administered and parenterally administered sodium salicylate upon chenodeoxycholic acid-induced colonic secretion. In our experiment, inoculation of four mM chenodeoxycholic acid into the rat cecum produced net secretion of water and sodium which was not reversed by preincubation of this bile acid with eight mM of sodium salicylate. Similarly, an intravenous bolus of either five mg of sodium salicylate per kg of body weight or 50 mg of sodium salicylate per kg of body weight failed to block salt or water secretion. Furthermore, 30 minute incubation of chenodeoxycholic acid with sodium salicylate produced neither reduction of in vitro aqueous bile acid concentration nor inhibition of ex vivo bile acid-facilitated hypotonic red cell hemolysis. These data suggest that sodium salicylate fails to sequester bile acids from aqueous solution and fails to block bile acid-mediated colonic secretion in the rat.
我们之前的研究表明,经肠腔给予大鼠水杨酸钠可阻断二羟基胆汁酸诱导的结肠分泌。在本研究中,采用体内大鼠盲肠袢技术,比较经肠腔给予和经肠外给予水杨酸钠对鹅去氧胆酸诱导的结肠分泌的影响。在我们的实验中,向大鼠盲肠接种4 mM鹅去氧胆酸会导致水和钠的净分泌,且预先将该胆汁酸与8 mM水杨酸钠共同孵育并不能逆转这种情况。同样,每千克体重静脉推注5 mg或50 mg水杨酸钠均未能阻断盐或水的分泌。此外,将鹅去氧胆酸与水杨酸钠共同孵育30分钟,既未降低体外胆汁酸的水溶液浓度,也未抑制离体胆汁酸促进的低渗红细胞溶血。这些数据表明,水杨酸钠无法从水溶液中螯合胆汁酸,也无法阻断大鼠胆汁酸介导的结肠分泌。