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  • 1
    Electronic Resource
    Electronic Resource
    Invited commentary (1981)
    Springer
    World journal of surgery 5 (1981), S. 173-174 
    Details
    ISSN: 1432-2323
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01658281
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  • 2
    Electronic Resource
    Electronic Resource
    Invited commentary (1979)
    Springer
    World journal of surgery 3 (1979), S. 603-604 
    Details
    ISSN: 1432-2323
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01654768
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  • 3
    Electronic Resource
    Electronic Resource
    Effect of a new potent H2-receptor antagonist on meal-stimulated gastric acid secretion and serum gastrin concentration in duodenal ulcer patients (1984)
    Springer
    Digestive diseases and sciences 29 (1984), S. 129-133 
    Details
    ISSN: 1573-2568
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We evaluated the effect of 20-, 40-, 60-, and 80-mg doses of SKF 93479, a new H2-receptor antagonist, on food-stimulated gastric acid secretion in duodenal ulcer patients. Medications were given as a single oral dose in the morning with a breakfast meal, and acid secretion was measured by in vivo intragastric titration in response to four blended steak meals infused into the stomach at intervals over a 24-hr period. A breakfast meal was infused immediately after medication; a luncheon meal was given 5 hr after drug, and a dinner meal was instilled 10 hr later. A second breakfast meal was infused 24 hr after medication. For comparison, the effect of 300 mg cimetidine, given as normally prescribed (with meals and at bedtime), on acid secretion was also studied. Food-stimulated acid secretion was inhibited in a dose-related manner by each of the four doses of SKF 93479. The antisecretory effect was most dramatic following the luncheon meal, and there was still significant (P〈0.05) inhibition of acid secretion at the dinner meal with all doses of SKF 93479. With the second breakfast meal 24 hr after medication, the 80-mg dose alone achieved significant (P〈0.05) inhibition of acid secretion. Inhibition of acid secretion was correlated positively with blood SKF 93479 levels. When compared with placebo results, serum gastrin concentration, measured 5 and 10 hr after medication, was significantly higher (P〈0.05) with SKF 93479.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01317053
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  • 4
    Electronic Resource
    Electronic Resource
    Overview of clinical cytoprotection (1985)
    Springer
    Digestive diseases and sciences 30 (1985), S. 81S 
    Details
    ISSN: 1573-2568
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01309390
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  • 5
    Electronic Resource
    Electronic Resource
    Cyclooxygenase inhibition with indomethacin increases human duodenal mucosal response to prostaglandin E1 (1989)
    Springer
    Digestive diseases and sciences 34 (1989), S. 1855-1859 
    Details
    ISSN: 1573-2568
    Keywords: human ; duodenum ; bicarbonate ; indomethacin ; prostaglandin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In humans, prostaglandins of the E1 class stimulate duodenal mucosal bicarbonate secretion, whereas the cyclooxygenase inhibitor, indomethacin, decreases both mucosal PGE2 and bicarbonate production. The purpose of this study was to determine whether a synthetic prostaglandin E1, enisoprost, diminished the inhibitory effects of indomethacin on mucosal bicarbonate secretion. In seven healthy subjects the proximal 4 cm of duodenum was isolated by occluding balloons. The isolated test segment was perfused with 154 mM NaCl (2 ml/min, 37° C). Each subject participated in four separate tests in random order. Indomethacin, 50 mg, or placebo was given 13 and 1 hr before testing. After measuring basal bicarbonate secretion, either 100 μg of prostaglandin E1 or placebo (in 154 mM NaCl) was perfused into the test segment over 30 min. As anticipated, PGE1 significantly increased duodenal mucosal bicarbonate secretion, and indomethacin decreased resting bicarbonate secretion. Indomethacin pretreatment significantly enhanced (P〈0.03 the mucosa's response to PGE1 compared to PGE1 alone. These results further support the observations that endogenous prostaglandins, in part, regulate human proximal duodenal bicarbonate secretion. Furthermore, suppression of endogenous prostaglandin generation results in an increased sensitivity of the duodenal mucosa to PGE1.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01536702
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  • 6
    Electronic Resource
    Electronic Resource
    Are anticholinergics plus antacids truly as effective as cimetidine plus antacids in the treatment of duodenal ulcer? (1982)
    Springer
    Digestive diseases and sciences 27 (1982), S. 385-387 
    Details
    ISSN: 1573-2568
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01295644
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  • 7
    Electronic Resource
    Electronic Resource
    Comparison of the serial dilution indicator and intragastric titration methods for measurement of meal-stimulated gostric acid secretion in man (1983)
    Springer
    Digestive diseases and sciences 28 (1983), S. 1001-1004 
    Details
    ISSN: 1573-2568
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Twoin vivo methods that permit quantitation of gastric acid secretion immediately after the meal are currently in use: intragastric titration and the serial dilution indicator method. During intragastric titration, intragastric pH is artifically maintained at 5.5 to 7 by the continuous addition of alkali to the gastric contents, while during serial dilution the intragastric pH is permitted to seek its natural pH. This study compared gastric acid secretion and serum gastrin in response to a liquid protein meal measured by both techniques in 10 subjects. Mean (±se) 3-hr acid outputs were almost identical (53.6±6.0 mmol/3 hr with intragastric titration and 52.0±8.5 mmol/3 hr with serial dilution indicator). Furthermore, 30 min secretory responses in individual subjects were highly correlated (r=0.98±0.01, P〈0.001). Also, in spite of intragastric pH being less than 1.5 by 90 min after the meal during the serial dilution method, total integrated serum gastrin concentrations after the meal were similar (intragastric titration=20.6±7.3 ng min/ml versus serial dilution indicator=23.5±9.8 ng min/ml) and individual 30-min gastrins during the two separate tests were highly correlated (r=0.80±0.06, P〈0.01). It is concluded that both meal-stimulated gastric acid secretion and serum gastrin concentrations as measured by intragastric titration and by the serial dilution indicator method produced similar results.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01311729
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  • 8
    Electronic Resource
    Electronic Resource
    Human proximal duodenal ion and water transport (1995)
    Springer
    Digestive diseases and sciences 40 (1995), S. 241-246 
    Details
    ISSN: 1573-2568
    Keywords: acetazolamide ; chloride ; lidocaine ; potassium ; potential difference ; prostaglandin E2 ; sodium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Intestinal ion transport is mediated by the interaction of enterocyte function, the enteric nervous system, humoral agents, and mucosal production of carbonic anhydrase. Our purpose was to examine the effect of the carbonic anhydrase inhibitor acetazolamide and inhibition of the enteric nervous system with the topical anesthetic lidocaine on basal and prostaglandin E2-stimulated ion and water transport and transmucosal electrical potential difference. At rest, mean basal (95% confidence intervals) net ion secretion into the human proximal duodenum was: Cl− 670 (288–1052), Na+ 818 (410–1225), K+ 32 (14–51) µmol/cm/hr. Basal net water transport was 30 (14.6–45.3) ml/hr, and the potential difference (PD) was 7.0 (3.6–10.9) mV, lumen negative. Intraluminal prostaglandin E2 increased the secretion of all ions, water, and the PD. After pretreatment with acetazolamide and luminal administration of lidocaine, basal ion transport was unchanged, but the response to luminal PGE2 was inhibited. It is concluded that: (1) at rest there is a net secretion of Na+, K+, Cl−, and water by the human proximal duodenum; and (2) PGE2-stimulated water electrolyte secretion is dependent in part upon mucosal carbonic anhydrase activity and the enteric nervous system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02065404
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  • 9
    Electronic Resource
    Electronic Resource
    Modulation of Bicarbonate Secretion in Rabbit Duodenum (The Role of Calcium) (1998)
    Springer
    Digestive diseases and sciences 43 (1998), S. 120-125 
    Details
    ISSN: 1573-2568
    Keywords: CALCIUM ; A23187 ; BICARBONATE ; CYCLIC ADENOSINE MONOPHOSPHATE ; VASOACTIVE INTESTINAL PEPTIDE ; PROSTAGLANDIN E2 ; CARBACHOL
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Surface epithelial bicarbonate secretionprotects the proximal duodenum from acid peptic injury.Cyclic adenosine monophosphate and calcium serve asintracellular mediators of intestinal transport.Experiments were performed to examine whether calciumparticipates in duodenal bicarbonate transport. Strippedduodenal mucosa from rabbits was studied in Ussingchambers. HCO3 - transport wasstimulated by the calcium ionophore A23187, carbachol, vasoactiveintestinal peptide, prostaglandin E2,dibutyryl-cyclic adenosine monophosphate, and electricalfield stimulation. A23187 stimulatedHCO3 - secretion andISC; tetrodotoxin failed to inhibit this effect. Thecalcium-channel blocker verapamil abolishedHCO3 - secretion stimulated bycarbachol, vasoactive intestinal peptide, and electricalfield stimulation, but failed to alter basal, prostaglandin E2- ordibutyryl-cyclic adenosine monophosphate-stimulatedHCO3 - secretion. Therefore,calcium is likely required during stimu lation ofduodenal epithelial HCO3 -transport by carbachol, vasoactive intestinal peptide, and electricalfield stimulation. Prostaglandin E2- anddibutyryl-cyclic adenosine monophosphate appear toactivate duodenal HCO3 - secretionby a calcium-independent pathway(s).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1018836407044
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  • 10
    Electronic Resource
    Electronic Resource
    Human Proximal Duodenal Alkaline Secretion Is Mediated by Cl-/HCO3- Exchange and HCO3- Conductance (1998)
    Springer
    Digestive diseases and sciences 43 (1998), S. 1205-1210 
    Details
    ISSN: 1573-2568
    Keywords: HUMAN ; BICARBONATE TRANSPORT ; CYCLIC AMP ; PROSTAGLANDIN E2 ; THEOPHYLLINE
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The proximal duodenal epithelium secretesbicarbonate into an adherent mucus layer, therebyprotecting the mucosa from injury by gastric acid andpepsin. While bicarbonate secretion is stimulated andinhibited by a number of agonists and antagonists, theapical anion transport pathways have not been addressedfully. The objective was to assess if apicalCl-/HCO3 - exchange andCl-:HCO3 - conductanceare involved in duodenal mucosal bicarbonate secretion(DMBS). In healthy volunteers, the proximal 4 cm ofduodenum was isolated, perfused with either saline or4,4′-diisothiocyano-2,2′-disulfonic acid(DIDS), and bicarbonate secretion and transepithelial potentialdifference (PD) were stimulated by eitherPGE2 or the phosphodiesterase inhibitortheophylline to increase cyclic AMP. Luminal DIDSabolished PGE2-stimulated DMBS, yet had no effect on the increase in PD andfailed to significantly alter theophylline-induced DMBSand PD. Therefore, in human proximal duodenum, itappears that PGE2 and cAMP activate distinctHCO transport pathways 2 likely involving a DIDS-sensitiveCl-/HCO3 - exchanger andDIDS-insensitive HCO3 -conductance.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1018895405362
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