Reference

Influence of blind loop on the pharmacokinetics of dopamine and sulfasalazine

Influence of blind loop on the pharmacokinetics of dopamine and sulfasalazine. Thithapandha, Amnuay (Fac.Several substances are used for example 144-83-2 and 102-32-9 which are their cas registry numbers. Sci., Mahidol Univ., Bangkok, Thailand). Pharmacol. Res. Commun., 9(3), 269-77 (English) 1977. CODEN: PLRCAT. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacodynamics) In order to test the formation of m-hydroxyphenylacetic acid (MHPAA) [621-37-4] from dopamine (I) [51-61-6] and the release of sulfapyridine [144-83-2] from sulfasalazine [599-79-1], self-filling blind loops were created in the jejuna of conventional rats. When dopamine (100 mg) was administered to both control and blind-loop animals, the ratio of MHPAA excreted in the 1st 24 h to that in the 2nd 24 h averaged 12.2 (range 3.8 to 44) in animals with blind loops and 0.09 (range 0 to 0.16) in controls. The presence of a blind loop did not affect the excretion of homovanillic acid [306-08-1] and dihydroxyphenylacetic acid [102-32-9], urinary metabolites of dopamine not derived from bacterial metab. A similar conclusion was also drawn from studies with sulfasalazine (10 mg). A significantly greater quantity of sulfapyridine was excreted in the 1st 6 h in rats with blind loops than in controls. These studies indicate that the presence of a blind loop of the rat's small intestine is assocd. with significant alteration in the kinetics of urinary excretion of flora dependent metabolites of dopamine and sulfasalazine. This observation might serve as the basis for a new method of detecting bacterial overgrowth. .

Effects of sulfasalazine and 5-aminosalicyclic acid on the human colonic prostaglandin system

Effects of sulfasalazine and 5-aminosalicyclic acid on the human colonic prostaglandin system. Peskar, Brigitta M. (Dep. Gastroenterol., Univ. Essen, Essen D-4300, Fed. 9030-87-9 and 9055-65-6 are also occured in this study. Rep. Ger.). Symp. Giovanni Lorenzini Found., 17(New Trends Pathophysiol. Ther. Large Bowel), 185-96 (English) 1983. CODEN: SGLFD9. ISSN: 0166-1167. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) In human colonic prepns., sulfasalazine (I) [599-79-1] inhibited prostaglandin synthetase [9055-65-6] activity at a low concn. of arachidonic acid (6 nmol/L) but stimulated PGE2 [363-24-6] formation at a high substrate concn. (60 mmol/L). In contrast, 5-aminosalicylic acid (II) [89-57-6], the I metabolite, inhibited prostaglandin synthetase at low as well as at high concns. of arachidonic acid. Both I and II inhibited the activity of 15-hydroxyprostaglandin dehydrogenase [9030-87-9], I being the more effective inhibitor. I inhibited the activity of D13-prostaglandin reductase [57406-74-3], whereas II had no effect. In intact human colonic mucosal cells, I increased the release of PGE2 and enhanced the formation of the metabolite 15-keto-13,14-dihydroPGE2 [363-23-5], indicating stimulation of prostaglandin formation. After prolonged incubation, however, mucosal release of PGE2 tended to be increased in the presence of decreased formation of its metabolite. II, on the other hand, inhibited mucosal release of PGE2 and its metabolite irresp. of the duration of the incubation period. The relation of these results to the treatment of inflammatory bowel disease with I is discussed. .