motilin and Duodenal-Ulcer

Topics: Biomarkers; Constipation; Diabetes Mellitus; Diagnostic Techniques, Endocrine; Diarrhea; Duodenal Ulcer; Gastrointestinal Motility; Humans; Inflammatory Bowel Diseases; Kidney Failure, Chronic; Motilin; Radioimmunoassay; Receptors, Gastrointestinal Hormone; Receptors, Neuropeptide; Reference Values; Specimen Handling

Topics: Adenoma, Islet Cell; Chenodeoxycholic Acid; Cholecystokinin; Cholelithiasis; Dehydration; Diabetes Mellitus; Duodenal Ulcer; Gastric Inhibitory Polypeptide; Gastrins; Gastrointestinal Hormones; Humans; Motilin; Pancreatic Neoplasms; Secretin; Syndrome; Vasoactive Intestinal Peptide; Zollinger-Ellison Syndrome

Topics: Adult; Digestion; Duodenal Ulcer; Duodenitis; Duodenum; Gastric Acidity Determination; Gastrointestinal Motility; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Motilin; Myoelectric Complex, Migrating; Stomach

Very few phase III activity of the interdigestive migrating contractions (phase III) occurs in the stomach of fasted duodenal ulcer patients. But the mechanism is not well understood. In this study, we studied the effect of gastric and duodenal acidification on the spontaneous phase III activity in the upper gastrointestinal tract of conscious dogs. Gastric and duodenal motor activity in 5 conscious dogs was monitored by means of chronically implanted force transducers. Intragastric pH changes were measured by placing a pH glass electrode in the gastric antrum. Intragastric and intraduodenal acidification was achieved by i.v. infusion of histamine, and by intragastric and intraduodenal instillation of acidic solutions of different pHs. The plasma motilin concentrations were measured by radioimmunoassay. Histamine (40 micrograms/kg/h) inhibited spontaneous phase III activity, but the histamine-induced inhibition was completely prevented by pretreatment with famotidine, a potent histamine H2 receptor antagonist (0.3 mg/kg, i.v.). Intragastric acidification at pH 1.0 strongly inhibited spontaneous phase III activity, but an acidic solution at pH 2.0 had no effect in inhibiting phase III activity. Intraduodenal acidification at pH 1.0 also inhibited spontaneous phase III activity. Histamine injection and gastric and duodenal acidification at pH 1.0 strongly suppressed motilin release. It is concluded that gastric and duodenal acidification at pH 1.0 inhibits the occurrence of the spontaneous phase III activity, and the suppression of endogenous release of motilin due to gastric and duodenal acidification at pH 1.0 is involved in this inhibitory mechanism.

Topics: Animals; Disease Models, Animal; Dogs; Duodenal Ulcer; Electrodes; Electrophysiology; Famotidine; Female; Gastric Acid; Gastrointestinal Motility; Histamine; Hydrogen-Ion Concentration; Male; Motilin; Muscle Contraction; Muscle, Smooth; Stomach Ulcer

Fourteen patients with duodenal ulcers and eight healthy volunteers were examined to measure interdigestive gastroduodenal motility and plasma motilin. In order to study the effects of gastric acid on the gastroduodenal motility, 20 mg of famotidine was administered intravenously. The motility index of the gastric antrum and the duodenum, as well as the pH in the duodenal bulb were calculated. The duodenal pH was significantly lower and the gastric motility index was significantly weaker before the duodenal interdigestive migrating complex (IMC) in the ulcer patients than in the controls. Motilin levels increased before the duodenal IMC and decreased afterwards in both groups. Famotidine significantly increased the duodenal pH and the gastric motility index before the IMC, but no changes in the motilin level were noted. We conclude that duodenal ulcer patients have duodenal hyperacidity that results from increased inflow from the antrum and antral hypomotility during the gastric IMC and that these changes are normalized by the administration of famotidine. These results suggest that gastric acid inhibits antral contraction during the gastric IMC.

Topics: Adult; Duodenal Ulcer; Duodenum; Famotidine; Female; Gastric Acid; Gastric Acidity Determination; Gastrointestinal Motility; Humans; Male; Motilin

Topics: Adult; Duodenal Ulcer; Duodenum; Female; Gastrointestinal Motility; Humans; Hydrogen-Ion Concentration; Male; Motilin

To further elucidate the pathophysiological role of peptide hormones in duodenal ulcer (DU) disease, several endocrine, paracrine and neurocrine peptides were determined radioimmunologically in biopsies of gastroduodenal mucosa obtained endoscopically in 8 subjects without upper gastrointestinal disease, and in 8 duodenal ulcer patients. The DU patients had a BAO of 6.6 +/- 1.9 and a PAO of 41.8 +/- 6.1 mEq/h. In DU patients, a lack of the acid and gastrin-release inhibiting agent somatostatin was found neither in antral nor in fundic mucosa (185 +/- 60 vs 83 +/- 19 pmol/g tissue wet weight in controls). Basal and peak acid outputs of DU patients were positively correlated with fundic somatostatin concentrations (p less than 0.01). While gastrin levels were not significantly elevated in the antrum of DU patients, the mucosal content of potentially releasable gastrin of the duodenal bulb and the descending duodenum was higher than in controls (p less than 0.01). In the whole duodenum, CCK-like immunoreactivity was also more abundant in DU patients than in controls, whereas GIP and motilin did not exhibit characteristic profiles. Presumably as a reactive phenomenon, the mucosal levels of the peptidergic neurotransmitters VIP and substance P were markedly increased in the proximal duodenum of DU patients.

Topics: Adult; Cholecystokinin; Duodenal Ulcer; Duodenum; Female; Gastric Inhibitory Polypeptide; Gastrins; Hormones; Humans; Intestinal Mucosa; Male; Middle Aged; Motilin; Somatostatin; Stomach; Substance P; Tissue Distribution; Vasoactive Intestinal Peptide

Changes in gastric acid secretion and plasma levels of CCK, gastrin, motilin, neurotensin and somatostatin in response to modified sham feeding (MSF) were investigated in 8 asymptomatic duodenal ulcer patients. MSF caused a significant increase in gastric acid secretion whereas the peripheral plasma concentrations of the various polypeptides remained unchanged. The study gives further support for the notion that MSF activates the vagal innervation to the parietal cells more selectively than insulin hypoglycaemia.

Topics: Adult; Aged; Cholecystokinin; Duodenal Ulcer; Food; Gastric Acid; Gastrins; Gastrointestinal Hormones; Humans; Middle Aged; Motilin; Neurotensin; Somatostatin

Interdigestive contractile activity in the gastrointestinal tract was measured in dogs and humans. During the interdigestive state, it was found that in healthy dogs and humans, cyclically-recurring strong contractions occurred in the stomach at approximately 100 min intervals and migrated through the small bowel in a caudal direction. The interdigestive contractions consist of three phases, phase I being quiescent while phases II and III are contractile. Phase II contractions resemble those in the digestive state and therefore mix the contents, and phase III contractions are strong in contractile force and consequently squeeze and expel the contents in a caudal direction. Intraduodenal pH changes were studied together with motor activity and it was found that intraduodenal pH remained at a slightly alkaline level during the interdigestive state in the dog; however, in human studies, it was revealed that intraduodenal pH drops below pH 7.0 only during the phase II period. These characteristic contractile changes in the interdigestive state are controlled at least in part by the cyclic increase in motilin concentration in the plasma, but it is not known what regulates the cyclic release of motilin during the interdigestive state. Feeding promptly eliminates changes in the plasma motilin concentration. It is not known whether other gut hormones are involved in the regulation of these specific motor changes in the interdigestive state. One of the typical disorders in motor activity was found in duodenal ulcer. In duodenal ulcer patients, the most characteristic difference from normal subjects was that the duration of phase II activity was significantly prolonged and intraduodenal pH fluctuated widely and intensely during the period. Hypersecretion of acid is well known to be the specific feature of this disease. However, the present study clearly indicates that spontaneous acid secretion per se or vagally induced acid secretion during phase II disturbs the interdigestive motor cycle and, in consequence, leads to the development of ulcers due to the fact that acid contents alone are continuously mixed in the stomach over the prolonged period of phase II activity. These findings lead us to a better understanding of the true pathogenesis of this disease as well as effective treatment of patients from a radical as well as symptomatic standpoint.

Topics: Adult; Animals; Digestion; Digestive System Physiological Phenomena; Dogs; Duodenal Ulcer; Food; Gastrins; Gastrointestinal Motility; Humans; Hydrogen-Ion Concentration; Motilin; Muscle Contraction; Secretin