Interrelationship between serum gastrin concentration, gastric acid secretion, and gastric emptying rate in recurrent peptic ulcer.
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Biomedical subjects
Publications and source records attributed to E Amdrup.
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Based on experience of a pilot series of 100 patients treated by parietal cell vagotomy (PCV) and a prospective clinical comparison between PCV (in some cases with drainage added) and selective gastric vagotomy (SGV) with drainage (D) or antrectomy (A) in some 900 patients, the following conclusions can be drawn: PCV is followed by virtually no sequelae. When drainage is added this is no longer the case and the results are the same as those following SGV + D. PCV and SGV + D show the same recurrence rate at 3 years (approx. 7%). Men do better than women after PCV but not after SGV + D. Preoperative gastric acid secretion had no predictive value in these studies. In non-obstructing duodenal ulcer the surgical choice appears to be between PCV (no sequelae) and SGV + A (no recurrence). The optimal operation for prepyloric ulcer cannot as yet be determined.
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Pressures in the Oddi sphincter and common bile duct were determined before, immediately after and several weeks after endoscopic papillotomy. Fifteen patients were included in the study. Significant decreases in Oddi sphincter and common bile duct pressures were found and the decrease in Oddi sphincter pressure was to some extent dependent upon the length of the papillotomy.
After excision of the oxyntic gland area in seven miniature pigs and cholecystogastrostomy in six of them, two developed chronic gastric ulcers in the gastric remnant. No parietal cells were found in the two pigs with ulcers, whereas small areas with polypoid oxyntic mucosa were found in four pigs without ulcer. The study indicates that bile-induced chronic gastric ulcer can occur in the pig despite the absence of oxyntic cells.
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The effect of surgical isolation and extrinsic denervation of the distal 5 to 7 cm of the human esophagus on resting gastroesophageal sphincter pressure and its response to graded increases of external abdominal compression was determined in 89 patients with duodenal ulcer. Fasting serum gastrin concentration also was measured. No significant changes in resting sphincter pressure were obtained before and after vagotomy of various types: parietal cell vagotomy, selective gastric vagotomy plus drainage, and selective gastric vagotomy plus precise antrectomy. No correlation between resting sphincter pressure and fasting serum gastrin concentration was found in any of the groups studied. The increase in gastroesophageal sphincter pressure was similar to the increase in intragastric pressure after 10, 20, and 30 mm Hg of external abdominal compression and was unchanged after all types of vagotomies. These results suggest that (1) extrinsic innervation of the lower esophageal sphincter in humans does not regulate the resting tone of the sphincter; (2) extrinsic "mechanical" influence does not play any role in the maintenance of resting pressure; (3) the effect of increased abdominal pressure is a pure mechanical effect, is unchanged after vagotomy, and therefore is not regulated by external neural reflex.
An easy, quick and practical way to determine the magnitude of gastric resection during operation consists of determining the length of the lesser and greater curvatures with a Nélaton's catheter. According to the extent of gastrectomy, different denominations should be used. If a precise antrectomy is desired, the physiologic antrum-corpus border should be determined.
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Gastroesophageal reflux was investigated in 80 patients with duodenal ulcer by analysis of symptomatology and the acid reflux test. Resting gastroesophageal sphincter pressure (GESP) and postvagotomy reduction in basal and pentagastrin stimulated gastric acid secretion were also studied. Reflux symptoms were present in 40% of the patients, and this incidence was significantly reduced two months after vagotomy. In patients studied late after operation reflux symptoms were still less frequent than before operation, but not significant. After vagotomy, no significant changes in the fasting GESP or in gastroesophageal reflux as determined by the pH glass electrode were demonstrated. Thus, the decrease in reflux symptoms may be explained by the significant reduction in gastric acid secretion. Denervation of the cardia and the lower esophagus does not influence GESP or gastroesophageal reflux.
Gastroesophageal sphincter pressure and serum gastrin concentration were determined in the fasting state and the intake of a protein food in 6 normal subjects, 6 patients with gastric ulcer, and in 6 patients with duodenal ulcer. No significant differences in the fasting state were found. After the food intake, gastroesophageal sphincter pressure increased significantly over basal values in normals and in patients with duodenal ulcer, but in patients with gastric ulcer a decrease in pressure was noted. Serum gastrin rose in all subjects studied after the food stimulation, but it was significant only in the gastric and duodenal ulcer group. In two normals and two patients with duodenal ulcer the ingestion of a potato meal similar in weight to the protein meal showed no change either in serum gastrin or in sphincter pressure. In one additional nromal and one duodenal ulcer, the constant intravenous infusion of Aminosol during 2 hours produced no change in serum gastrin or sphincter pressure. These results indicate that the effect of protein food on sphincter pressure is different for gastric or duodenal ulcers; furthermore, that this effect is mediated by proteins in the gastrointestinal tract.
Gastroesophageal sphincter pressure (GESP) and serum gastrin concentration (SGC) were determined in the basal state and after a protein meal in 6 patients with duodenal ulcer (DU) 6 patients after parietal cell vagotomy (PCV) 6 patients after selective gastric vagotomy plus drainage (SGV + D), and 6 patients after selective gastric vagotomy plus precise antrectomy (SGV + A). No correlation in the resting state between GESP and SGC was observed. After food ingestion, DU patients showed a sustained rise in GESP which lasted up to the end of the experiment. The vagotomized patients, however, showed no rise in sphincter pressure after food intake--rather a tendency to decrease in pressure occurred. On the contrary, SGC rose significantly after food ingestion in patients with SGV + D or PCV, while in DU patient this rise was less significant. Patients with vagotomy and antrectomy showed no rise in SGC. These results do not suggest that SGC and extrinsic vagal innervation in the resting state play a significant role in the maintenance of the tone of GES. After food ingestion an interaction may occur between intact vagal innervation and rise in SGC in order to obtain an adequate rise in GESP.
Gastroesophageal sphincter pressure and serum gastrin concentration were determined in the fasting state and after the intake of a protein food in 6 normal subjects, 6 patients with gastric ulcer, and in 6 patients with duodenal ulcer. No significant differences in the fasting state were found. After the food intake, gastroesophageal sphincter pressure increased significantly over basal values in normals and in patients with duodenal ulcer, but in patients with gastric ulcer a decrease in pressure was noted. Serum gastrin rose in all subjects studied after the food stimulation, but it was significant only in the gastric and duodenal ulcer group. In two normals and two patients with duodenal ulcer the ingestion of a potato meal of similar weight to that of the protein meal showed no change either in serum gastrin or in sphincter pressure. In one additional normal subject and one duodenal ulcer patient the constant intravenous infusion of Aminosol for 2 h produced no change in serum gastrin or sphincter pressure. These results indicate that the effect of protein food on sphincter pressure is different for gastric or duodenal ulcers, and, furthermore, that this effect is mediated by proteins in the gastrointestinal tract.