Mean Peak Acid Output Research Articles

Functional Characteristics of Duodenal Ulcer Patients and Their First-Degree Relatives

The behaviour of acid secretion, serum pepsinogen I and II (PG I and PG II) and morphology of the gastric mucosa were analyzed in 59 duodenal ulcer probands (DU probands), their 199 first-degree relatives and 228 control subjects. DU probands had as a rule antral gastritis with normal or slightly altered corpus mucosa, and higher mean peak acid output (PAO), PG I and II levels than their relatives and controls. Sibs of DU probands differed from their controls mainly with regard to morphology which showed features characteristic of DU probands, i.e. antral gastritis with normal or slightly altered corpus mucosa. Moreover, high PAO levels were found highly significantly more often in sibs of DU probands (13%) than in controls (6%). Likewise, the prevalence of endoscopic signs of active or past duodenal ulcer were present in sibs highly significantly more often than in controls and they accumulated in the subgroup of sibs with high PAO or PG I levels. It seems probable that the occurrence of high PAO and PG I levels in sibs of DU probands can be considered as signs of increased liability to duodenal ulcer. PAO and PG I were as expected significantly higher in male than in female probands, relatives and controls. Exclusion of cases of corpus gastritis decreased the levels but the sex difference persisted. PAO, PG I and II revealed a significant increase of the levels in middle age followed in older age in case of PAO and PG I by a significant decrease. The decrease was abolished when the cases of corpus gastritis were excluded suggesting an effect of gastritis. However, the earlier increase of the levels remained virtually unaffected although there was a uniform decrease of the mean values. This suggests the participation of factors unrelated to gastritis. The nature of the factors remains unknown, but literature data and data derived from our recent study suggest involvement of anatomical factors such as an increase in the size of acid and PG I secreting area.

Effect of intragastric infusions of ethanol and wine on serum gastrin concentration and gastric acid secretion

The effects of ethanol and wine oil serum gastrin concentration and gastric acid secretion were evaluated in 13 normal volunteers. Solutions studied were pure ethanol (5%, 12%, and 36%), red wine, and white wine. Each solution contained 28 g of ethanol and each was administered as a slow, steady intragastric infusion to simulate normal ingestion of beverages. When compared to saline (control), none of the pure ethanol solutions increased serum gastrin concentration or gastric acid secretion significantly. In contrast, red and white wine (12% ethanol vol/vol) were potent stimulants of gastrin release and acid secretion when compared either to saline or pure 12% ethanol. Mean (±SEM) peak serum gastrin increases with 300 ml of red wine, white wine, saline, and pure 12% ethanol were 253 ± 125, 182 ± 91, 13 ± 2, and 11 ± 3 pg/ml, respectively (p < 0.05 for red and white wine versus saline or 12% ethanol), and the mean peak acid outputs were 28.6 ± 2.8, 27.9 ± 1.9, 9.3 ± 2.0, and 11.9 ± 1.3 mmol/h, respectively (p < 0.05 for red and white wine versus saline or 12% ethanol). We conclude that red and white wine stimulate gastric acid secretion, probably by enhanced release of gastrin, and that this effect is not due to the ethanol content of wine.

Acid secretion from the completely isolated blood perfused canine stomach.

1. The canine gastric arterial supply was isolated and perfused by means of an extracorporeal circuit. The gastric venous blood was returned to the dog's venous system. Histamine acid phosphate (20 microgram min-1) infused intra-arterially gave a mean peak acid output of 2.3 m-mole per 10 min. 2. When a plateau of acid secretion was observed, the gastric venous blood was diverted to the oxygenator, by-passing the dog entirely (vascular isolation). This resulted in an immediate decrease in acid output which fell to or near zero by 90 min after isolation. 3. In three dogs, part of a lung was perfused in series with the stomach before total isolation of the gastric vasculature. With histamine stimulation, acid secretion was observed for about 1 hr with a peak acid output of 0.5 m-mole per 10 min during the period of total isolation. 4. Indomethacin (10 mg kg-1) was given to five dogs approximately 1 hr before vascular isolation. After acid secretion reached a plateau (mean peak acid output 2.3 m-mole per 10 minutes), the gastric circulation was isolated by diverting the gastric venous blood to the oxygenator. Acid secretion was maintained for 50 min, after which it gradually declined to reach 30% of the peak value after 2 hr. 5. Indomethacin (10 mg kg-1) and methysergide bimaleate (1 mg) were given I.V. to five dogs approximately 1 hr before vascular isolation. After acid secretion reached a plateau (peak output 3.0 m-mole per 10 min), the gastric circulation was isolated by diverting the gastric venous blood to the oxygenator. The plateau of secretion was maintained for a further 2 hr with no inhibition. 6. Methysergide bimaleate given alone did not prevent the inhibition of secretion caused by the total vascular isolation of the stomach. 7. These results suggest that in the isolated canine stomach preparation naturally occurring inhibitors of gastric acid secretion, which are normally metabolized at least in part in the lungs, accumulate in the circulation and may account for the observed suppression of acid secretion.

Gastric ulcer: effect of healing on gastric acid secretion and fasting serum gastrin levels.

In 15 patients with uncomplicated gastric ulcers, basal and peak gastric acid outputs and fasting serum gastrin levels were studied before and after healing. The mean basal acid output [4.0 +/- 1.3 (SEM) mEq H+/hr], the mean peak acid output (29.5 +/- 5.1 mEq H+/hr), and the mean fasting serum gastrin level (80.3 +/- 16.7 pg/ml) in these patients did not change significantly with healing. Failure of gastric secretory function to change with healing suggests that mucosal resistance factors are more important than gastric acid secretion in the pathogenesis of a gastric ulcer.

Gastric acid secretion in chronic atrophic gastritis and chronic (superficial) gastritis.

Basal and pentagastrin-stimulated peak acid outputs were determined in 21 subjects with chronic atrophic gastritis and 10 subjects with chronic superficial gastritis. All subjects were Caucasian. The histological diagnosis was based on multiple gastric biopsy specimens obtained through a fibregastroscope. Comparison of the results with those of a previously reported Caucasian control group show that the mean basal acid outputs of subjects with chronic (superficial) gastritis were significantly higher than that of controls and subjects with chronic atrophic gastritis. No significant difference was found in the mean peak acid outputs of controls and subjects with chronic atrophic gastritis or chronic (superficial) gastritis.

Effect of atropine and proximal gastric vagotomy on the acid response to fundic distension in man.

In four healthy subjects and in 12 patients with duodenal ulcer (DU), graded balloon distension of the gastric fundus and body caused increments in acid output related to the distension volumes. The mean peak distension response amounted to about 50% of the mean peak acid output (PAOpg) evoked by intravenous infusion of pentagastrin in a dose of 300 microng/h, eliciting maximum observed secretory response. During distension with the largest balloon volume, 1-0 mg atropine injected intravenously significantly depressed the acid secretory rate, the median inhibition amounting to about 80%. In two patients with DU, 2-5 mg atropine completely abolished acid secretion during fundic distension. In nine subjects with DU, complete proximal gastric vagotomy profoundly depressed the secretory responses to graded fundic distension, eliminating the acid response to the smallest balloon volume used. A slight, but significant, response to the largest distension volume persisted after complete vagotomy. Incomplete proxomal gastric vagotomy was found to reduce only moderately the distension responses in five patients, and the peak acid response to fundic distension as related to PAOpg remained unchanged. In conclusion, distension of the gastric fundus and body in man stimulates acid secretion by means of an atropine-sensitive, presumably cholinergic, reflex mechanism and the findings after vagotomy are in agreement with the concept that this reflex mechanism is conveyed by both short intramural and long vagovagal pathways.

Effect of smoking on gastric acid secretion.

Summary: The effect of smoking on gastric acid secretion was studied in 16 smokers and 16 non-smokers. The basal, smoking, and peak acid outputs were determined. Statistical analysis showed the following results: No significant difference was found between the mean basal acid output and mean smoking acid output, in both smokers and non-smokers. The mean peak acid output was significantly much higher than both the mean basal and smoking acid out-puts, in smokers and non-smokers. There was no significant difference in the mean basal, smoking, and peak acid outputs between smokers and non-smokers. When the difference between basal and smoking acid outputs were considered in each individual case, however, the smoking acid output tended to be lower than basal in smokers, but higher than basal in non-smokers. This difference was just significant. It is concluded that while smoking has no significant effect on gastric acid secretion in smokers and non-smokers, there appears to be a significant difference in the gastric secretory response to smoking between smokers and non-smokers.

Gastric Acid Secretion in Patients with Duodenal Ulcer.

Augmented histamine tests were performed in 349 patients with duodenal ulcers verified by operation, of whom 268 were men between 16 and 84 years of age, and 81 were women between 12 and 78 years; all were citizens of Copenhagen. In the men the mean peak acid output was 44 mEq H+ per hour, ranging from 16.8 to 111.4 mEq. The mean acid output in women was 32.3 mEq H+ per hour, ranging from 13.7 to 74.4 mEq. In men with duodenal ulcer a statistically significant correlation between age and peak acid output is clearly demonstrable, the acid output decreasing by 5 mEq H+ per hour for each ten years' increase of age. In women, the acid output falls about two mEq H+ per hour per decade, although the statistical significance of this finding is not certain.