Effects of cimetidine and ranitidine on interdigestive and postprandial lower esophageal sphincter pressures and plasma gastrin levels in normal subjects

Smout, Andreas J.; Bogaard, J W; Hattum, Jan van; Akkermans, L.M.A.

doi:10.1016/0016-5085(85)90521-9

Cited by 34 publications

(6 citation statements)

References 22 publications

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“…In summary, proton-pump inhibitors or histamine H 2 antagonists are widely used in the therapy of gastroesophageal reflux disease (GERD) patients but neither omeprazole nor cimetidine and ranitidine had any significant effect on lower esophageal sphincter (63,64), and ranitidine does not resolve the primary dysfunction of the pyloric sphincter or esophagitis after tube insertion into the rat pyloric sphincter. Therefore, in prolonged esophagitis disorders, as it resolves the primary dysfunction of the pyloric sphincter, the pentadecapeptide BPC 157, together with its interactions with other sphincter controlling systems and cytoprotective function [i.e., somatosensory neurons, NO, dopamine, serotonin (6,7,56,57)], could also be therapeutically considered.…”

Section: Discussionmentioning

confidence: 99%

Prolonged Esophagitis After Primary Dysfunction of the Pyloric Sphincter in the Rat and Therapeutic Potential of the Gastric Pentadecapeptide BPC 157

et al. 2007

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Abstract. Seven or fourteen days or twelve months after suturing one tube into the pyloric sphincter (removed by peristalsis by the seventh day), rats exhibit prolonged esophagitis with a constantly lowered pressure not only in the pyloric, but also in the lower esophageal sphincter and a failure of both sphincters. Throughout the esophagitis experiment, gastric pentadecapeptide BPC 157 (PL 14736) is given intraperitoneally once a day (10 µg / kg, 10 ng / kg, last application 24 h before assessment), or continuously in drinking water at 0.16 µg / ml, 0.16 ng / ml (12 ml / rat per day), or directly into the stomach 5 min before pressure assessment (a water manometer connected to the drainage port of a Foley catheter implanted into the stomach either through an esophageal or duodenal incision). This treatment alleviates i) the esophagitis (macroscopically and microscopically, at either region or interval), ii) the pressure in the pyloric sphincter, and iii) the pressure in the lower esophageal sphincter (cmH 2 O). In the normal rats it increases lower esophageal sphincter pressure, but decreases the pyloric sphincter pressure. Ranitidine, given using the same protocol (50 mg / kg, intraperitoneally, once daily; 0.83 mg / ml in drinking water; 50 mg / kg directly into the stomach) does not have an effect in either rats with esophagitis or in normal rats.

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Section: Discussionmentioning

confidence: 99%

Prolonged Esophagitis After Primary Dysfunction of the Pyloric Sphincter in the Rat and Therapeutic Potential of the Gastric Pentadecapeptide BPC 157

et al. 2007

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“…Aim-To investigate the gastrointestinal motor mechanisms involved in the hyperglycaemia induced retardation of gastric emptying in patients with type I diabetes mellitus and autonomic neuropathy. In eight diabetic patients antroduodenal manometry was performed simultaneously with scintigraphic measurement of emptying of a mixed solid-liquid meal, during euglycaemia (5-8 mmol/l glucose) and hyperglycaemia (16)(17)(18)(19) mmol/l glucose), on separate days, in random order. Results-Hyperglycaemia decreased the cumulative antral motility index from 38-3 (range 24.2-47.6) to 30-8 (range 17.3-38.1) (p=0.025) and reduced the number of antral pressure waves propagated over .4-5 cm (p=0.04).…”

Section: Introductionmentioning

confidence: 99%

“…In all patients gastric emptying and antroduodenal motility were measured simultaneously during euglycaemia (5-8 mmol/l) and hyperglycaemia (16)(17)(18)(19) mmol/l), on two separate days at a one week interval and in random order.…”

Section: Introductionmentioning

confidence: 99%

Gastrointestinal motor mechanisms in hyperglycaemia induced delayed gastric emptying in type I diabetes mellitus.

Samsom¹,

Akkermans²,

Jebbink³

et al. 1997

Gut

151

107

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“…Cimetidine was used to remove the effect of hydrogen ion interfer ence during these studies. It has been shown that this Ht blocker does not alter reflux of total bile acids into the stomach [8] and the interdigestive migrating motor complex which is closely related to DGR has been found not to be altered [9][10][11].…”

Section: Discussionmentioning

confidence: 99%

Continuous Monitoring of Sodium Ion Concentration in the Human Stomach – A New Technique for the Detection of Duodenogastric Reflux

Smythe¹,

Bird²,

Johnson³

1992

Digestion

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Measurement of sodium ion concentration in gastric juice offers a simple .means of detecting duodenogastric reflux (DGR). Using aspirated gastric juice, we measured sodium ion concentration, bile acid levels and phospholipase A² activity and found that sodium ion levels increase along with these other standard markers during DGR. Following this, using a sodium ion selective electrode and a portable data logger, continuous recordings of sodium ion concentration were made in the human stomach. These studies demonstrated the ability of sodium ion monitoring to detect major DGR episodes in the body of the stomach.

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Effects of cimetidine and ranitidine on interdigestive and postprandial lower esophageal sphincter pressures and plasma gastrin levels in normal subjects

Cited by 34 publications

References 22 publications

Prolonged Esophagitis After Primary Dysfunction of the Pyloric Sphincter in the Rat and Therapeutic Potential of the Gastric Pentadecapeptide BPC 157

Prolonged Esophagitis After Primary Dysfunction of the Pyloric Sphincter in the Rat and Therapeutic Potential of the Gastric Pentadecapeptide BPC 157

Gastrointestinal motor mechanisms in hyperglycaemia induced delayed gastric emptying in type I diabetes mellitus.

Continuous Monitoring of Sodium Ion Concentration in the Human Stomach – A New Technique for the Detection of Duodenogastric Reflux

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