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The author describes a very rapid and accurate method of determining the acidity of gastric juice which is based on recent findings. Starting from the electrometrically determined pH value and the volume of the gastric juice, the actual hydrogenion concentration may be read from a table. The laboratory work is considerably simplified by this method.
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Dogs were provided with oesophageal fistulae, fully innervated pouches of the fundic stomach and the duodenal bulb, and a gastric cannula. Gastric secretion was stimulated by sham feeding for 10 min. The bulbar pouches were perfused either with 0.9 per cent NaCl or with 0.1 N HCl. Plasma gastrin concentrations were determined by radioimmunoassay. Bulbar acidification effectively inhibited gastric acid secretion. Plasma gastrin responses were not suppressed. Instead, plasma gastrin concentrations were higher than in controls. The results show that the bulbar mechanism does not inhibit gastric acid secretion by reducing gastrin release.
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Prevention of acute gastric erosions with histamine H2-receptor blocking agents suggests that these drugs may improve the ability of the gastric mucosa to maintain electrical, ionic, and protein concentration gradients. In 5 awake mongrel dogs, transmural potential difference, ion fluxes, and protein loss were measured across Heidenhain pouches topically exposed to isotonic solutions containing either 80 mM HCl or 80 mM HCl plus 20 mM sodium taurocholate (BS). The dogs received an intravenous infusion of either saline (as a control) or the H2 antagonist metiamide, 10 mumoles per kg-hr. Metiamide increased the H+ clearance rate found after acid test solution exposure but had no significant effect on potential difference or ion fluxes. H2 antagonism decreased the protein loss but not the increase in cation permeability due to BS. Net H+ loss actually increased, which, along with a decrease in Cl- gain, suggests inhibition of acid secretion by metiamide in BS-exposed gastric mucosa. These effects of metiamide point to histamine as a likely mediator of the gastric mucosal damage due to BS.
Better knowledge of the physiology of gastric acid secretion and especially the effects of insulin on the secretion, permits better definition of the indications for gastric functional investigation after vagotomy. The most reliable estimation of the effects of vagotomy is obtained by determining, before and after, the basal acid secretion, the maximal and post-insulinic secretions. The results should be expressed as hourly output and not in relation to arbitary criteria based on the titratable acid of the gastric juice. This investigation may be used to determine the quality of vagotomies carried out on a group of patients and to compare series of subjects in which different types of vagotomy were carried out. The tests at present available do not, however, determine precisely the effects of vagotomy in a particular patient. Their use for drawing up individual prognosis has not been demonstrated but their value is far from negligible in the diagnosis of recurrence.
As reported previously, gastrin-stimulated gastric secretion in the dog and in man was suppressed by an intravenous infusion of secretin, These results, both in the dog and in man, also were obtained by introduction of acid into the duodenum, which indicated that both endogenous and exogenous secretion inhibit gastrin-stimulated gastric secretion at the oxyntic cell level. Feeding a test meal in man gave rise to an increase of plasma gastrin, reaching a peak of 120 pg. per milliliter at 15 minutes after feeding and remaining above control level for 2 to 3 hours. Is was found that plasma gastrin was suppressed greatly during the intravenous infusion of pure secretin. In animal experiments endogenous gastrin release produced by irrigation of the antral pouch also inhibited both endogenous and exogenous secretin. These results indicate that secretin inhibits gastrin release at the G-cell level in the antrum. On the other hand, it also was observed that endogenous gastrin release ceased when the pH of the perfusate dropped below 2.5. The following conclusions are drawn from the above findings. (1) Gastrin release is suppressed primarily by direct contact of acid with the antrum. The feedback mechanism in this case operates intraluminally in the stomach. (2) The low pH content of the stomach stimulates the release of secretin from the duodenum. The secretin released in this way not only inhibits gastric acid secretion at the oxyntic cell secretin released in this way not only inhibits gastric acid secretion at the oxyntic cell secretin released of gastrin at the G-cell level in the antrum. The level but also blocks the release of gastrin at the G-cell level in the antrum. The feedback mechanism brought about by acid of gastric origin occurs through the general circulation.
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Twenty-one patients (4 females and 17 males) were re-examined 20 years after partial gastrectomy for benign peptic ulcer. Different stages of morphological change in the gastric stump mucosa were compared with haematological parameters as well as with gastric acid and IF secretions. Biopsy specimens were taken by the direct vision technique. Haematological values including also serum vitamin B12, folate and Schilling test were determined. Gastric acid and IF secretions were lower in all patients with "selective parietal cell atrophy" in the gastric mucosa compared with those of other patients. Serum B12 and Schilling test values showed the same tendency. The present study indicates that it is possible to determine the gastric function dependent on parietal cells according to morphological criteria.
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The authors report the results of examination of 80 patients with ulcerous disease of the stomach and duodenum prior to and in the immediate period, as well as in 85 patients in late terms after typical Hofmeister-Finsterer gastrectomy. The acid-production of the stomach and its stump was studied by intragastric pH-metry, pepsine in the gastric juice was determined and also the resected stomach excretory function was studied by fibrochromogastroscopy. It is shown that the method of intragastric pH-metry is more advanrageous, since it gives an estimation of acid-production of the resected stomach in the immediate postoperative period, in particular.
1. Gastric acid responses to the test meals were measured in the Heidenhain pouch, gastric and pancreatic fistula dogs, using the intragastric titration method, and monitoring the rate at which a solution of 1-0 N-NaOH had to be added to maintain the pH of the gastric content constant at pre-selected values ranging from 5-0 to 1-0. In this way the pH profile of the gastric acid and pepsin responses to a liver extract meal kept in the Heidenhain pouch or gastric fistula as well as to exogenous stimuli such as histamine, pentagastrin or Urecholine could be determined. 2. A liver extract meal adjusted to pH 5-0 produced a potent and pressure-related stimulation of acid secretion from the Heidenhain pouch without any change in secretion from the main stomach and pancreas or in the serum concentration of immuno-assayable gastrin. 3. Graded decrease of the liver extract meal pH to below 5-0 resulted in the pH-dependent inhibition of gastric acid output, which at pH 1-0 was only about 30% of the value attained at pH 5-0. Acid secretion from the Heidenhain pouch induced by exogenous stimuli such as histamine, pentagastrin or Urecholine also showed gradual decrease when the pH of the pouch content was decreased in sequential order from 5-0 to 1-0. This pH-dependent inhibition was accompanied by an increase in pepsin secretion. 4. The pH-dependent inhibition of the Heidenhain pouch response to the liver extract meal was not altered by topical application of a local anaesthetic and atropine or by the intravenous infusion of large doses of atropine, secretin or metiamide, which were shown to cause a marked inhibition of the main stomach response to the liver meal. 5. The results indicate that there is a local and gastrin-independent inhibition mechanism of gastric acid secretion activated by an acidified meal making contact with the oxyntic gland area.
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The effect of carbenoxolone on taurocholate-induced changes in gastric mucosal permeabiity was assessed in three dogs, each of which was prepared with an antrectomy and a vagally denervated gastric pouch. Perfusion of the canine pouches with sodium taurocholate (40 mM) was associated with an increase in hydrogen ion back diffusion. This effect was not diminished by 10 days of carbenoxolone treatment. The effect of carbenoxolone on ethanol-induced changes in gastric mucosal permeability was assessed in six normal human subjects. A significant increase of gastric mucosal permeability was observed in six normal human subjects after instillation of ethanol (20 percent v/v). After 3 weeks of oral ingestion of carbenoxolone, there was inconsistent protection against ethanol-induced increases in gastric mucosal permeability. Basal secretion of hydrogen ion and postethanol hydrogen ion secretion appear to be diminished by carbenoxolone. These studies suggest that carbenoxolone does not protect against taurocholate- and ethanol-induced increases in gastric mucosal permeability in the dog and in man. It seems unlikely that carbenoxolone exerts its beneficial effect on the healing of gastric ulcers in man by an effect on gastric mucosal permeability.
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