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Background and Aim: The aim of this study was to determine whether the gastric longitudinal shortening occurs during the gastric phase III in man. Methods: Intragastric pH and gastroduodenal motility were simultaneously measured by means of a 24-h ambulatory recording system in 14 healthy volunteers. In nine subjects (group A), the catheter assembly was endoscopically clipped to the gastric mucosa with the middle transducer and the distal pH sensor in the antrum. In the remaining five subjects (group B), measurements were performed without securing the assembly. Results: In 23 of the 25 gastrointestinal interdigestive migrating complexes in group A, the distal and middle transducers showed characteristic duodenal contractions (11–12 c.p.m.). Neutralization was noted at the distal pH sensor. Similar phenomena were observed during all 15 gastrointestinal interdigestive migrating complexes in group B. The catheter assemblies escaped into the duodenum despite the fact that they were secured to the stomach. This may be explained by gastric longitudinal shortening during gastric phase III activities. Conclusions: Studies of intragastric physiology with test catheters must take the effect of gastric longitudinal shortening during phase III into consideration. [ABSTRACT FROM AUTHOR]

To simplify assessment of gastric emptying, we have developed a radiopaque barium marker method. The subjects were 11 healthy volunteers, 30 patients with progressive systemic sclerosis, 16 patients with dysmotility-like dyspepsia, 7 patients with irritable bowel syndrome, and 6 patients with diabetes mellitus. We tested three types of radiopaque markers with manometry by a three-channel strain gauge transducer. The 4.5-mm ring-shaped markers with a specific gravity of 1.2 were emptied from the stomach in correlation with the number of high-amplitude (>50 mm Hg) antral contractions. The percentage of residual markers at 2 hr was significantly (P < 0.05) lower in patients with irritable bowed syndrome than in normal controls, and at 5 hr it was significantly (P < 0.05) higher in patients with systemic sclerosis with esophageal dysmotility, dysmotility-like dyspepsia, or diabetes than in normal controls. This radiopaque barium marker method may be useful as a screening test for determining whether gastric emptying is rapid or delayed. [ABSTRACT FROM AUTHOR]

The role of Helicobacter pylori infection in the development and exacerbation of reflux esophagitis was investigated. The prevalence of Helicobacter pylori infection, the severity of atrophic gastritis, and esophageal motility (determined by esophageal manometry by an infusion catheter method) were assessed in patients with mild (n = 46) and severe (n = 27) reflux esophagitis and subjects without reflux (n = 28). Compared with the prevalence of Helicobacter pylori infection in the non-reflux group, the prevalence in the mild and severe reflux groups (60.7%, 47.8%, and 14.8%, respectively) was significantly (P < 0.05) lower. Atrophic gastritis was milder in both reflux groups than in the non-reflux group. The degree of gastritis was also milder in the severe reflux group than in the mild reflux group. The esophageal sphincter pressure was significantly (P < 0.05) lower in the reflux groups than in the non-reflux group, and the amplitude of primary peristalsis was significantly (P < 0.05) lower in the severe reflux group than in the non-reflux group. There were no significant differences between reflux patients with and without Helicobacter pylori infection in the parameters of esophageal manometry. These data imply that a low prevalence of Helicobacter pylori infection may result in a milder grade of atrophic gastritis, and consequently, exacerbate reflux esophagitis. [ABSTRACT FROM AUTHOR]

Objective: To investigate interdigestive gastroduodenal motility with an infused catheter and measure plasma motilin levels in eight normal individuals and 18 patients with dysmotility-like dyspepsia. Methods and Results: All normal individuals had normal gastroduodenal interdigestive migrating complexes. Patients with dysmotility-like dyspepsia were classified into three subgroups on the basis of gastric antral motility: 1) seven patients with normal interdigestive migrating complexes, 2) five patients without interdigestive migrating complexes and with gastric phase II predominant over phase I, and 3) six patients without interdigestive migrating complexes and with phase I predominance. The maximum and mean plasma motilin levels were significantly different in normal individuals from those in subgroup 3 (Kruskal-Wallis test, p < 0.05). Conclusions: Dysmotility-like dyspepsia appears to be a heterogeneous condition. Abnormal motilin secretion may cause dysmotility in subgroup 3, but dyspepsia in subgroup 1 and the absence of interdigestive migrating complexes in subgroup 2 could not be explained only on this basis. [ABSTRACT FROM AUTHOR]

It is known that there is a close relationshipbetween serum motilin fluctuation and the initiation ofgastric interdigestive migrating complexes (IMC) (1).The administration of synthetic motilin initiates IMC (2), and antimotilin serum blocks theinitiation of IMC (3). Erythromycin has recently beenshown to be a motilin-receptor agonist (4), and motilinreceptors have been found in the human stomach (5). At present motilin is considered to initiateIMC through both the vagal cholinergic pathway anddirect stimulation of smooth muscle. From the clinicalpoint of view, Labo et al (6) and our group (7) recently reported on the relationship between a lowmotilin concentration and disturbance of IMC in patientswith dyspepsia. On the other hand, little is known aboutthe effect of an abnormally high motilin concentration on gastroduodenal motility. We have found threeoutpatients in our clinic at Gunma University Hospitalwith duodenal ulcer or duodenitis who had disturbedinitiation of IMC despite an abnormally high plasma motilin concentration. [ABSTRACT FROM AUTHOR]

The advent of histamine H receptor antagonists (H-RA) has allowed the treatment of reflux esophagitis (RE) to be controlled over a relatively long term. The authors have experienced some cases resistant to H-RA, but it was revealed that these cases can be successfully treated with proton pump inhibitors. It has been suggested that esophagogastric dysmotility can lead to RE. RE has been treated for many years by using GI-prokinetic agents, which theoretically inhibit acid reflux and improve esophageal acid clearance. In order to compare the effects on acid reflux of an H-RA (famotidine), a proton pump inhibitor (omeprazole) and a GI-prokinetic agent (cisapride), we measured the 24-hour pH in the esophagus and stomach simultaneously, before and after treatment in 17 patients with RE. It was found that the proton pump inhibitor was the most effective drug for inhibiting esophageal acidification, followed by famotidine and then cisapride. Furthermore, we found that cisapride often actually exacerbated acid reflux. The differences in inhibitory effects on acidification allowed us to draw conclusions regarding the treatment of RE. It was concluded that the stronger the inhibitory effect of a drug on acid secretion, the more useful it was in the treatment of RE. The GI-prokinetic drug did not inhibit acid reflux as much as we had expected. [ABSTRACT FROM AUTHOR]

The effects of famotidine on human upper gastrointestinal motility were investigated, together with the relationship of gastric alkalinization and serum gastrin levels to changes produced by famotidine. Intravenous famotidine (20 mg), at a dose level in which an inhibitory effect on acetylcholinesterase activity is not recognized, was given to 13 patients with progressive systemic sclerosis but no other disorders. Gastric phasic motor activity was not changed significantly, but the lower esophageal sphincter pressure was elevated significantly in comparison with 15 controls given physiological saline, even when gastric phasic motor activity was taken into consideration. Gastric alkalinization with 7% sodium bicarbonate did not significantly increase the sphincter pressure in all 7 subjects so treated. No significant correlation was recognized between the serum gastrin level, the lower esophageal sphincter pressure, and the gastric motility index in any of the 3 groups. It was, therefore, concluded that intravenous administration of famotidine affected upper gastrointestinal motility, especially the lower esophageal sphincter pressure, through an as yet unknown mechanism other than inhibition of acetylcholinesterase activity, gastric alkalinization, or elevation of serum gastrin levels. [ABSTRACT FROM AUTHOR]

The relationship between interdigestive gallbladder and gastroduodenal motilty simultaneously with the behavior of plasma motilin and CCK levels in 20 subjects was investigated. We used an infusion catheter method for the measurement of gastroduodenal motility, and real-time ultrasonography for the measurement of gallbladder size. In gastric phase II, the gallbladder contracted with extension of the major axis and shrinking of the minor axis, with its minimum volume being 84% of the volume in phase I. The gallbladder then filled rapidly assuming a sphere-like shape with extension of the minor axis and shrinking of the major axis in gastric phase I. This motility was recognized only during the gastrointestinal interdigestive migrating complex (GI-IMC) cycle, originating in the stomach, and was associated with an increase of motilin levels, it was not seen before or after the intestinal IMC (I-IMC), which originated in the duodenum without contraction of the stomach or an increase of motilin levels. Furthermore no apparent relationship was recognized between CCK and gastric or gallbaldder motility. Our findings suggest that gallbladder motility in the interdigestive period has a close relationship with gastroduodenal motility and is related to the appearance of the GI-IMC. [ABSTRACT FROM AUTHOR]

Abstract A 22-year-old man was unable to belch. He could sense intraesophageal gas, but had no chest pain. An upper gastrointestinal X-ray series and endoscopic examination showed no abnormalities. Esophageal manometry showed normal relaxation of both the upper and lower esophageal sphincters with primary peristalsis during deglutition. However, bolus injection of air into the middle esophagus failed to initiate the belch reflex. [ABSTRACT FROM AUTHOR]

Presents a case study of a patient with diffuse esophageal spasm who obtained successful relief of chest pain and dysphagia with beta-adrenoreceptor agonists. Clinical history of the patient; Results of laboratory examinations administered; Treatment.

We report a rare case of benign esophagobronchial fistula associated with achalasia. The fistula healed spontaneously after esophagocardioplasty with a gastric patch, suggesting the utility of this procedure. [ABSTRACT FROM AUTHOR]

A gastric atypical epithelium, which has been known as a precancerous state for a long time, does not seem to need a surgical resection according to our present studies. [ABSTRACT FROM AUTHOR]