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Studies of basal and peak acid output with an augmented histamine test.

On the basis that the most repeatable measurement of acid output of the stomach is the peak half hour after an augmented dose of histamine, the author suggests a modification of the Kay test, including titration of the gastric juice to neutrality and measurement of the chloride concentration. The aspiration tube was sited fluoroscopically. It is suggested that the ;peak half hour' should be substituted for the period 15-45 minutes after administration of histamine. This modification is supported by the presented data. It should be noted, however, that the titration technique has also been modified. The ranges of basal and maximum gastric secretion (volume, acidity, acid output, parietal and non-parietal components) in 20 normal males and 20 normal females are presented and analysed for differences of age and sex. Both basal and maximum (histamine stimulated) gastric secretion declined with age, more so in women than in men. ;Maximum' gastric secretion was greater in men than in women, especially in older subjects.

Chlorides↗

Effect of three single doses of oxmetidine administered intravenously on the volume and acidity of gastric secretion, serum prolactin and gastrin concentration in healthy volunteers.

Gastric acid secretion was measured in six healthy volunteers following the intravenous administration (over 30 min.) of oxmetidine 200 mg, 400 mg and 800 mg in a randomized double blind trial for 12 hours. Gastric aspirates were fractionated into hourly aliquots and pH, volume, gastric acidity and gastric acid output were determined. Total gastric acid output over 12 hours was significantly reduced from 24.4 mmol/12 h (median) after placebo to 13.5 mmol/12 h, 11.8 mmol/12 h and 7.7 mmol/12 h after oxmetidine 200 mg, 400 mg and 800 mg respectively. An inhibition of at least 90% was achieved with all doses of oxmetidine and this lasted dose-dependently for 4 to 6 hours. A rise in pH to greater than 5 occurred during the 2nd or 3rd hour after dosing which lasted for 2-5 hours depending on the dose administered. Mean hourly pH was dose-dependently significantly higher for 4-6 hours following oxmetidine treatment than after placebo. A significant reduction in gastric acidity after oxmetidine infusion was also observed while the reduction in volume output calculated for 12 hours was not statistically significant. No significant rises in serum gastrin levels were observed with the oxmetidine doses used. Three out of the six subjects tested showed an increase in serum prolactin levels in response to the highest dose of oxmetidine but this was not statistically significant. The results of the present study have shown that the administration of 400 mg oxmetidine did not cause a longer pH elevation greater than 5 than 200 mg, while with 800 mg side effects were observed in one of the six subjects studied.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

A canine model for the study of gastric secretion and emptying after a meal.

Our aim was to develop a chronic canine model that would serve for the simultaneous measurements of postprandial gastric secretion and emptying by a double-marker dilution technique without artificially interfering with intragastric pH. A constant duodenal perfusion of a nonabsorbable marker allowed determination of luminal flow and total recovery of a second marker ingested with a meal. By calculating the amount of meal marker remaining in the stomach and its dilution (by repeat gastric sampling), we could determine the volume of gastric contents. Acid concentration in gastric samples was measured by titration ex vivo, and gastric acid content was calculated by multiplying the volume of gastric contents by titratable acidity. In this model, net acid gain at each sampling interval indicates acid output. Acid and volume losses are equivalent to duodenal acid load ad emptying rate, respectively. The method has been validated by virtually abolishing the endogenous secretion of acid (by intravenous infusion of cimetidine) and the calculation of known volumes and concentrations of acid exogenously instilled in the animal's stomach. Our results indicate that this is an accurate and practical method for the physiologic measurement of postprandial gastric function in dogs. Further, these studies substantiate the validity of the assumptions upon which the human double-marker method was based.

Animals↗

Pentagastrin-stimulated gastric acid secretion: does desensitization exist?

The existence of tachyphylaxis to pentagastrin-stimulated gastric acid secretion in humans is controversial. To study this, we determined gastric acid output in 19 duodenal ulcer patients following the administration of two successive intramuscular injections of pentagastrin (6 micrograms/kg body weight). In 18 of 19 patients, the maximal acid output decreased by 33.73 +/- 3.25% (mean +/- SE) following the second pentagastrin administration when compared with the maximal acid output following the first injection. This study indicates the existence of tolerance to pentagastrin-induced gastric acid secretion in humans, which may be due to a receptor-mediated phenomenon of "down-regulation."

Adult↗

Increased plasma gastrin levels in connection with inhibition of gastric acid responses to sham feeding following bulbar perfusion with acid in dogs.

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.

Animal Feed↗