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BACKGROUND/AIM: Gastric emptying is a major cause of variability when studying gastrointestinal parameters as a function of time. Here, we investigate whether the parametric variability could be reduced by running experiments on a gastric emptying basis rather than on a time basis. METHODS: Healthy volunteers were intubated with gastric and duodenal tubes and were given a liquid meal containing polyethylene glycol to monitor gastric emptying. Gastric pH and human gastric lipase (HGL) concentrations were measured. Their variations were plotted as a function of either time or gastric emptying (%). In both cases, mean curves of variation were established by polynomial regression. RESULTS: When time was the variable used, the overall deviation of the experimental values from the values given by the best-fitting curve was high (chi2 = 33 for gastric pH; chi2 = 1,744 for HGL), and the individual deviations increased with time. When gastric emptying was the variable used, the overall deviation of the experimental values from the values given by the best-fitting curve was much lower (chi2 = 10 for gastric pH; chi2 = 642 for HGL). CONCLUSIONS: Expressing gastric pH or HGL concentration as a function of gastric emptying instead of time makes it possible to reduce the individual variability. This new type of data analysis may be of a general interest to observe specific variations of gastrointestinal parameters induced by drugs, hormones, and meals, and that might be masked by the large intrinsic variability induced by gastric emptying. Copyright 2001 S. Karger AG, Basel
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11549836&dopt=Abstract
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Aliment Pharmacol Ther. 2001 Sep;15(9):1445-52.
Influence of anti-Helicobacter triple-therapy with metronidazole, omeprazole and clarithromycin on intestinal microflora.
Buhling A, Radun D, Muller WA, Malfertheiner P.
State Institute of Hygiene Saxony-Anhalt, Magdeburg, Germany.
BACKGROUND: Proton pump inhibitor-based therapy including two antibiotics is the treatment of choice for Helicobacter pylori infection. Oral antibiotic treatment can lead to intestinal overgrowth of potentially pathogenic bacteria. AIM: To investigate the intestinal microflora before and at different times after H. pylori treatment with omeprazole, clarithromycin and metronidazole. METHODS: Bacterial growth in faecal samples from 51 patients infected with H. pylori was determined qualitatively and quantitatively. During the same period of time, stool samples from 27 H. pylori-negative controls were taken and investigated at the same intervals. RESULTS: The microflora of H. pylori-infected patients was different from that in H. pylori negative controls. It was characterized by a high concentration of lactobacilli, mainly Lactobacillus acidophilus. Immediately after therapy there was an increased colonization with yeasts, while the growth of lactobacilli and other species was inhibited. Clostridium difficile was cultured from three cases, but without clinical manifestations of pseudomembranous colitis. After 4 weeks of therapy, the microflora returned to normal and was not different from that of the H. pylori-negative control group. CONCLUSIONS: In H. pylori-positive patients the intestinal flora is characterized by an increase in growth of acid-tolerant L. acidophilus. Eradication therapy exerts only a short-term influence on intestinal flora, whereas in the long term, the intestinal microflora is restored to a pattern similar to that of the control group.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11552917&dopt=Abstract
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Am J Physiol Gastrointest Liver Physiol. 2001 Oct;281(4):G870-7.
Intragastric pH regulates conversion from net acid to net alkaline secretion by the rat stomach.
Coskun T, Chu S, Montrose MH.
Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA.
Our previous report showed gastric mucosal surface pH was determined by alkali secretion at intragastric luminal pH 3 but by acid secretion at intragastric pH 5. Here, we question whether regulation of mucosal surface pH is due to the effect of luminal pH on net acid/base secretions of the whole stomach. Anesthetized rats with a gastric cannula were used, the stomach lumen was perfused with weakly buffered saline, and gastric secretion was detected in the gastric effluent with 1) a flow-through pH electrode and 2) a fluorescent pH-sensitive dye (Cl-NERF). During pH 5 luminal perfusion, both pH sensors reported the gastric effluent was acidic (pH 4.79). After perfusion was stopped transiently (stop-flow), net acid accumulation was observed in the effluent when perfusion was restarted (peak change to pH 4.1-4.3). During pH 3 luminal perfusion, both pH sensors reported gastric effluent was close to perfusate pH (3.0-3.1), but net alkali accumulation was detected at both pH sensors after stop-flow (peak pH 3.3). Buffering capacity of gastric effluents was used to calculate net acid/alkaline secretions. Omeprazole blocked acid secretion during pH 5 perfusion and amplified net alkali secretion during pH 3 perfusion. Pentagastrin elicited net acid secretion under both luminal pH conditions, an effect antagonized by somatostatin. We conclude that in the basal condition, the rat stomach was acid secretory at luminal pH 5 but alkaline secretory at luminal pH 3.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11557506&dopt=Abstract
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