Digestive diseases and sciences
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Randomized Controlled Trial Clinical Trial
Oral naloxone antagonizes loperamide-induced delay of orocecal transit.
Orocecal transit time was determined by the lactulose hydrogen breath test in nine healthy volunteers after administration of placebo, loperamide (16 mg per os), and loperamide (16 mg per os) followed by oral naloxone at doses of 16 and 32 mg. The four tests were performed in double-blind conditions and in random sequences. Transit time (mean, SD) after loperamide (128.8 min, 32.9) was significantly increased (P less than 0.05) compared with placebo (85.5 min, 35.7), loperamide followed by naloxone 16 mg (88.8 min, 46.2), and loperamide followed by naloxone 32 mg (84.4 min, 40.6). These results show that the peripheral opioid agonist loperamide delays orocecal transit in healthy subjects and that naloxone per os at adequate doses antagonizes this effect.
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Theories on the etiology of Crohn's disease have included extrinsic agents and intrinsic bowel wall defects. We sought to determine the presence of immunoreactive antigens specific to Crohn's disease tissue by modifying the enzyme-linked immunosorbent assay. Tissue proteins were extracted from four patients with Crohn's disease and from four normal segments of colon from patients with colonic cancer. ⋯ These Crohn's disease sera also showed preferential recognition of glycoproteins extracted from Crohn's disease tissue compared to glycoproteins from normal colonic tissue (P less than 0.0005). The nature of these immunoreactive proteins, whether extrinsic or intrinsic, is not yet known. The ELISA may help in further characterization of Crohn's disease tissue-specific glycoprotein(s) and to develop a clinically useful serological test.
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Role of local motility changes in the pathogenesis of duodenal ulcers induced by cysteamine in rats.
The possible role of local motility in the pathogenesis of duodenal ulcers was investigated in rats using cysteamine. Duodenal motor activity was measured as intraluminal pressure recordings by means of a balloon positioned in the proximal duodenum. Subcutaneous administration of cysteamine (100 mg/kg) produced two linear bandlike lesions in the proximal duodenum within 6 hr. ⋯ The enhanced duodenal motility induced by cysteamine was blocked partially by atropine and only slightly by 16,16-dmPGE2. Dopamine showed a dose-dependent inhibition on the duodenal hypermotility following cysteamine, and at 30 mg/kg almost completely abolished the development of contractions. These results suggest that abnormal hypermotility in the duodenum may be partly involved in the pathogenesis of cysteamine-induced duodenal ulcers.
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The effect of cisapride, a new gastrokinetic drug, on gastroduodenal motility was tested in six healthy volunteers. In order to obtain a model for slowed gastric emptying, dopamine was infused at a rate of 8 micrograms/kg/min. Dopamine significantly slowed the fractional emptying rate of fasting gastric contents from 5.14 +/- 0.37 to 1.45 +/- 0.67 %/min. ⋯ When given on a dopamine background, however, both metoclopramide and cisapride decreased bile salt reflux below control values without any active treatment. It is concluded that emptying of fasting gastric contents can be speeded by cisapride, particularly when emptying is slowed by dopamine. A clear effect on bile salt reflux cannot be demonstrated.