Acid Output In Response Research Articles

Inhibition of Histamine-Stimulated Gastric Acid Secretion by Hydrogen Sulfide in Male Rats

Recently, hydrogen sulfide (H_2S) introduces as the third gaseous transmitter that has many physiologic and pharmacologic roles in the body. The aim of the present study was to investigate the effect of exogenously given H_2S on histamine-induced gastric acid secretion in rats. Thirtytwo male Wistar rats (150-200 g) were randomly assigned into 4 groups (8 per group). Animals were deprived of food but not water 24 h before the experiment and were randomly assigned into two control groups, distention-, and histamine-stimulated groups, and two NaHS-treated groups. To evaluate the effect of H_2S on histamine-induced gastric acid secretion, one group of animals were received an I.V. bolus of NaHS (a H_2S donor) at 80 μg/kg. To investigate the possible involved mechanism of the antisecretory effect of NaHS, mRNA expression of histidine decarboxylase (HDC) were evaluated by reverse-transcriptase PCR. The gastric acid output in response to histamine decreased by NaHS treatment (P＜0.01). Also the results showed that the level of gene expression of HDC was higher in NaHS-treated group than in control rats. The findings showed that the inhibitory effect of H_2S on gastric acid secretion was not related to a decrease in histamine release. It seems that up-regulation of HDC mRNA expression is secondary to inhibition of gastric acid secretion by NaHS.

Antisecretory Effect of Hydrogen Sulfide on Gastric Acid Secretion and the Involvement of Nitric Oxide

The present study was designed to investigate the effect of H2S on distention-induced gastric acid secretion. Fifty-two rats were randomly assigned to seven experimental groups. The gastric acid secretion was stimulated by gastric distention. Two groups of rats received L-cysteine or saline for 5 days before stimulation of the gastric acid secretion. Two groups of animals also received NaHS or saline just prior to stimulation of the gastric acid secretion. The effect of L-NAME and propargylglycine was also investigated. The mucosal levels of the gene expression of cyclooxygenase-2 (COX-2), endothelial nitric oxide synthase (eNOS), and H+/K+-ATPase α-subunit were quantified by qPCR and luminal concentrations of NO were determined. NaHS and L-cysteine decreased the gastric acid output in response to distention. The mRNA expression of H+/K+-ATPase α-subunit decreased by NaHS and L-cysteine as compared with the control group while gene expression of eNOS and COX-2 was upregulated. The inhibitory effect of NaHS on distention-induced gastric acid secretion was mitigated by pretreatment of L-NAME. These findings suggest the involvement of NO in mediating the antisecretory effect of H2S.

Urine acid output as a test of completeness of vagotomy

Peak acid output in response to sham feeding and changes in urine acid output 2 and 3 hours after a test meal have been measured in 20 normal volunteers, 17 asymptomatic patients after vagotomy, six patients with recurrent duodenal ulcer after vagotomy and ten normal subjects given a 48-h course of ranitidine, 150 mg 12-hourly. Gastric peak acid output in normal volunteers ranged from 6.9 to 22.1 mmol/h. All asymptomatic patients after vagotomy had a peak acid output less than 7 mmol/h, consistent with complete vagotomy. Five patients with recurrent ulcer had a peak acid output greater than 8 mmol/h, suggesting an incomplete vagotomy. Urine acid output after a test meal, expressed as the change from the basal rate of acid output, was always in a negative direction in normal subjects (fall in acid output = postprandial alkaline tide). This change was abolished in patients with complete vagotomy, in whom urine acid output increased after a meal. In five patients with incomplete vagotomy (and one other with recurrent ulcer and unknown vagal status) the urine acid output changed in a negative direction after a test meal. The relationship of urine acid output to gastric secretion was confirmed by the abolition of the postprandial alkaline tide in normal subjects given ranitidine. The results in patients with incomplete vagotomy did not overlap with those from patients with complete vagotomy. This suggests that this test could be used for the routine postoperative assessment of completeness of vagotomy.

Treatment of gastric ulcer by highly selective vagotomy without a drainage procedure: an interim report.

Abstract Fourteen patients with gastric ulcer alone and 5 patients with combined gastric and duodenal ulceration- have been treated by highly selective (parietal-cell) vagotomy without a drainage procedure (H.S.V.) the past 3 years. Before operation no evidence of gastric stasis was found, clinically, radiologically, or during tests of gastric secretion. Spontaneous acid out was low. Acid output in response to a test meal of meat extract was also found to be low. There no evidence that in the patients with gastric ulcer alone the ulcer was due to pyloric channel disease with excessive release of gastrin by the antrum. Each gastric ulcer was proved by frozen-section examination to be benign at the time of operation. Problems with gastric stasis were encontered in early postoperative period. The vagotomy was shown to be complete on insulin testing in each of 17 patients tested. Follow-up ranges from 1 month to 3 years. The clinical progress of the patients has been good, and has symptoms suggestive of recurrent ulceration gastric retention. Barium-meal examination in 11 patients who were follwed up for more than 9 months showed satisfactory gastric emptying, without recurrent ulceration. While the need for much longer follow-up is obvious, these preliminary results are encouraging. Further trial of H.S.V. for gastric ulcer, preferably in the form of a prospective, randomized comparison with Billroth-I gastrectomy, now seems desirable.

Perturbations in gastric physiology in Helicobacter pylori duodenal ulcer: are they all epiphenomena?

The Holy Grail of physiological studies in acid secretion has been to identify a specific abnormality in gastroduodenal physiology responsible for the development of duodenal ulcer disease. We review the available data relating duodenal ulcer and Helicobacter pylori infection to perturbations in gastric physiology, especially acid secretion. It is known now that elevated serum pepsinogen levels, reduced inhibition of acid secretion with antral acidification or distention, exaggerated gastrin response to meals or infusion of bombesin or gastric-releasing peptide, exaggerated acid output in response to gastric-releasing peptide, and abnormalities in duodenal bicarbonate secretion in response to instillation of acid are reversible epiphenomena related to the H. pylori infection and are not in themselves responsible for duodenal ulcer disease. H. pylori is inhibited by bile, yet can thrive in the duodenal bulb of duodenal ulcer patients. Glycine-conjugated bile acids are precipitated by acid; thus, any mechanism that would increase the duodenal acid load may remove the inhibitory bile and allow unrestrained growth of H. pylori. These data and speculations offer one possible explanation for why duodenal ulcer occurs in only some people--those with high acid secretion--and suggest that the combination of high duodenal acid load and H. pylori infection is sufficient to result in duodenal ulcer disease.

Gastrin-evoked secretion of pancreastatin and histamine from ECL cells and of acid from parietal cells in isolated, vascularly perfused rat stomach. Effects of isobutyl methylxanthin and α-fluoromethylhistidine

The ECL cells in the rat stomach release pancreastatin and histamine in response to gastrin stimulation. The present study compares the release of pancreastatin and histamine from the ECL cells and the secretion of acid from the parietal cells in response to gastrin, and examines how a markedly reduced histamine content in the ECL cells will affect the gastrin-evoked release of pancreastatin and the secretion of gastric acid. Totally isolated, vascularly perfused stomachs were prepared from fasted rats. Some of the rats had been pre-treated for 24 h with (α-fluoromethylhistidine (α-FMH), resulting in 80% depletion of oxyntic mucosal histamine (mainly ECL-cell histamine). The stomachs were perfused with rat gastrin-17, α-FMH, isobutyl methylxanthine (IBMX), or vehicle in various combinations for 8 h. The venous outflow was collected (30-min samples) for determination of histamine and pancreastatin-like immunoreactivity (LI) and the gastric luminal outflow was collected for determination of H +. Gastrin raised the outflow of pancreastatin-LI and histamine but did not raise the acid output unless IBMX was added. The outflow of pancreastatin-LI and histamine was greater after gastrin + IBMX (at least during the first 4-h period) than after gastrin alone. α-FMH reduced gastrin-evoked histamine outflow but did not affect gastrin-evoked pancreastatin-LI outflow. Also the acid output in response to gastrin + IBMX was much reduced by α-FMH. In conclusion, increased levels of intracellular cAMP enhanced the gastrin-evoked release of pancreastatin-LI and histamine from the ECL cells and made it possible for histamine, released from the ECL cells, to cause acid secretion from the parietal cells. ECL-cell histamine depletion reduced the gastrin-evoked acid secretion; it did not affect the gastrin-evoked release of pancreastatin-LI.

Gastrin-evoked secretion of pancreastatin and histamine from ECL cells and of acid from parietal cells in isolated, vascularly perfused rat stomach. Effects of isobutyl methylxanthin and α-fluoromethylhistidine

The ECL cells in the rat stomach release pancreastatin and histamine in response to gastrin stimulation. The present study compares the release of pancreastatin and histamine from the ECL cells and the secretion of acid from the parietal cells in response to gastrin, and examines how a markedly reduced histamine content in the ECL cells will affect the gastrin-evoked release of pancreastatin and the secretion of gastric acid. Totally isolated, vascularly perfused stomachs were prepared from fasted rats. Some of the rats had been pre-treated for 24 h with (α-fluoromethylhistidine (α-FMH), resulting in 80% depletion of oxyntic mucosal histamine (mainly ECL-cell histamine). The stomachs were perfused with rat gastrin-17, α-FMH, isobutyl methylxanthine (IBMX), or vehicle in various combinations for 8 h. The venous outflow was collected (30-min samples) for determination of histamine and pancreastatin-like immunoreactivity (LI) and the gastric luminal outflow was collected for determination of H+. Gastrin raised the outflow of pancreastatin-LI and histamine but did not raise the acid output unless IBMX was added. The outflow of pancreastatin-LI and histamine was greater after gastrin + IBMX (at least during the first 4-h period) than after gastrin alone. α-FMH reduced gastrin-evoked histamine outflow but did not affect gastrin-evoked pancreastatin-LI outflow. Also the acid output in response to gastrin + IBMX was much reduced by α-FMH. In conclusion, increased levels of intracellular cAMP enhanced the gastrin-evoked release of pancreastatin-LI and histamine from the ECL cells and made it possible for histamine, released from the ECL cells, to cause acid secretion from the parietal cells. ECL-cell histamine depletion reduced the gastrin-evoked acid secretion; it did not affect the gastrin-evoked release of pancreastatin-LI.

New non-invasive test of gastric acid secretion for use in children.

Loss of the gastric acid barrier may lead to recurrent enteric infections, small intestinal bacterial overgrowth, persistent diarrhoea, and thus malnutrition. To investigate this possibility, a new, non-invasive test of gastric acid secretion was developed ideal for field use in the developing world, where chronic diarrhoea and undernutrition are common. The test relies on the capacity of the kidney to retain H+ during gastric acid secretion, leading to a post-prandial urine 'alkaline tide'. Gastric intubation studies of seven healthy adult volunteers showed a direct relation between changes in gastric acid secretion and changes in urine acid output (measured as the H+/creatinine molar ratio in spot urine samples). Subjects who secreted gastric acid in response to stimulation with a sham feed showed a fall in urine acid output > 0.5 mmol H+/mmol creatinine (range -7.4 to -1.52 mean -1.12). The most reproducible decrease in urine acid output in response to normal food was observed around the time breakfast was usually eaten and was abolished by 36 hours of treatment with ranitidine. Breakfast time reductions in postprandial urine acid output in 22 healthy English children were comparable with those in healthy adults, and significantly different from values in achlorhydric adults. They were much more variable, however, in 106 Gambian children in whom values spanned both normochlorhydric and achlorhydric ranges (-12.7 to +1.8). Measuring changes in urine acid output at breakfast time provides a reliable indirect measure of gastric acid secretion that can be used in field conditions, enabling the relation between gastric acid output and the development of diarrhoeal diseases to be investigated.

Gastric acid secretion, parietal cell sensitivity, and endoscopic characteristics of duodenal ulcer patients with and without stigmata of recent bleeding

Duodenal ulcer patients with stigmata of recent hemorrhage are at high risk of rebleeding. Whether the acid secretory capacity, the parietal cell sensitivity and endoscopic characteristics are different in patients with and without stigmata of recent hemorrhage are unclear. To investigate these, we studied 885 patients with active duodenal ulcer. Among them 693 patients presented with pain only and the rest with gastrointestinal bleeding. Within the latter group, 135 patients had no or minor stigmata (i.e., flat spot) of bleeding while 37 patients had major stigmata of bleeding (i.e., visible vessel and visible clot). The basal acid output and gastric acid output in response to infusion of graded doses of pentagastrin from 93.8 to maximal dose of 6000 ng/kg.hour (maximal acid output) were measured. The dose of pentagastrin required for half maximal response to gastric acid output was taken to represent the sensitivity of the parietal cells to pentagastrin (D50c). The results demonstrated that the basal acid output, maximal acid output, and D50c were not significantly different among the three groups. Endoscopically the size and site of the ulcer were similar, but patients with major stigmata of bleeding had significantly higher degrees of duodenal inflammation and deformity. We conclude that gastric acid secretion and D50c were not significantly different in patients with major and minor stigmata of recent bleeding, indicating that gastric acid may not play a significant role in precipitating gastrointestinal bleeding.

Role of gastrin, histamine, and acetylcholine in the gastric phase of acid secretion in anesthetized rats.

To determine the relative contributions of gastrin, histamine, and cholinergic stimulation to the gastric phase of acid secretion, peptone-stimulated acid output was measured in urethan-anesthetized pylorus-ligated rats after intravenous administration of gastrin monoclonal antibody, cimetidine, and atropine. Intragastric peptone stimulated acid secretion four-fold over basal, which was associated with a significant increase in plasma gastrin levels. Gastrin immunoneutralization and simultaneous H2- and muscarinic-receptor blockade demonstrated that approximately 40% of peptone-stimulated acid output as attributed to endogenous gastrin through a histamine-dependent pathway, whereas 20% of acid output was accounted for by a cholinergic component. Another 10% of titratable acid was omeprazole-insensitive and presumably due to intragastric digestion of peptone. Therefore, approximately 30% residual acid output in response to peptone could not be accounted for by known acid stimulatory mechanisms. In rats given somatostatin monoclonal antibody to block the tonic inhibitory effect of endogenous somatostatin, residual acid output was a similar fraction of meal-stimulated acid output. In contrast, gastric distension induced by intragastric instillation of saline stimulated acid secretion to 1.5-fold over basal. Although 60% of distension-induced acid secretion could be inhibited by either H2 blockade or gastrin immunoneutralization, acid output returned to basal levels after simultaneous muscarinic blockade. These results indicate that gastrin, through a histaminergic pathway, is the principal mediator of meal-stimulated acid secretion in anesthetized rats. Approximately 30% of acid output was due to other unidentified mechanisms, such as chemical secretagogues, a direct effect of amino acids, or novel peptides.

Chronic nicotine intake increases the responses to muscarinic receptor stimulation.

Chronic nicotine administration depresses the autonomic ganglia, but its effects on the muscarinic receptors at the neuroeffector sites remain unclear. The present study, using rats, examines the influence of chronic treatment with nicotine (25 micrograms/ml drinking water) for 10 or 15 days on muscarinic receptor responses, as reflected by bethanechol-evoked gastric secretion or by acetylcholine-induced decreases in mean blood pressure. Bethanechol, 0.4, 0.8, 1.6 or 3.2 mg/kg injected subcutaneously, dose-dependently increased the basal gastric secretory volume and acid output in pylorus-ligated control animals which normally drank tap water. Rats given nicotine in their drinking water for 10 or 15 days showed a further marked increase in both the volume of gastric secretion and acid output in response to bethanechol injections. Although bethanechol dose-dependently increased acid secretion, the ulcer index was very small and there was no significant difference between the control and nicotine-treated groups. The basal mean blood pressure remained normal after the 10-day nicotine treatment. Acetylcholine, 0.1, 0.3, 1 or 3 micrograms/kg given intravenously, decreased the mean blood pressure; this acetylcholine-evoked blood pressure fall was intensified by nicotine pretreatment. The findings suggest that the responses to muscarinic receptor stimulation are increased by chronic nicotine treatment for 10 or 15 days. These exaggerated effects are possibly the consequence of persistent autonomic ganglion blockade by chronic nicotine treatment.

Action of beer and its ingredients on gastric acid secretion and release of gastrin in humans

The intragastric action of beer and its known ingredients before and after fermentation on gastric acid secretion and release of gastrin was studied in healthy humans. None of 11 tested ingredients of fermented beer (2 × 500 mL, pH 5.5, given either alone or in combination) or hop extract had any significant effect. Finished beer (6 weeks old) and new beer were potent stimuli of acid output, causing 93% and 76% of the incremental maximal acid output in response to pentagastrin (6 μg/kg SC), respectively. Before the addition of yeast, preproducts of beer were considerably less potent. Thus, first and finished wort caused only a minor acid response which was 48% and 46% of maximal acid output. Foreign fermentation in first and finished wort is presumably the reason for the stimulatory action because glucose solutions in concentrations (11.5% wt/vol) seen in wort did not stimulate acid secretion. However, glucose solutions to which yeast was added, resulting in fermentation, were as potent stimuli of acid secretion as beer. Lyophilization of beer at pH 11.0 and dialysis (cutoff mol wt, 1000) removed the stimulatory substances. The plasma gastrin responses paralleled the gastric acid response to the different stimulants. It was concluded that (a) the addition of yeast to finished wort and the following alcoholic fermentation are the essential steps for the stimulatory action of beer on gastric acid secretion and release of gastrin; (b) carbohydrate metabolites with a molecular weight of less than 1000 are the acid-stimulatory agents in fermented beer; and (c) gastrin is the mediator of the stimulation of acid secretion because all substances that had a potent acid-stimulatory action also were potent stimuli of gastrin release.

Vagal influences on gastric acid secretion in response to gastric distension in the ferret

The role of the vagus nerve in the stimulation of gastric acid secretion was investigated by comparing the acid output in response to gastric distension during augmented secretion mediated by electrical vagal stimulation and pentagastrin. Under control conditions distension increased acid output from 29.8 ± 3 μmol/10 min to 59.9 ± 5.5 μmol/10 min ( P < 0.0001). Bilateral cervical vagotomy significantly reduced both basal acid secretion and the response to distension although the increase during distension was still significant. Electrical vagal stimulation augmented basal acid output and the response to distension, and at 1 Hz both parameters were not different from that before vagotomy. However, the sensitivity of the response to distension was unchanged by vagal stimulation. Pentagastrin infusion augmented basal acid secretion and the response to distension in a similar manner to vagal stimulation. We conclude that the vagus nerves potentiate the gastric acid secretory response to distension not by facilitating enteric reflexes but by an action at the level of the parietal cell.

Fasting gastric pH and its relationship to true hypochlorhydria in humans

Abnormally low rates of gastric acid secretion (hypochlorhydria) are associated with bacterial overgrowth, enteric infection, and with hypergastrinemia and an increased risk of gastric neoplasms. In the present study, we evaluated the ability of fasting gastric juice pH measurements to detect true hypochlorhydria. True hypochlorhydria was defined as a peak acid output in response to a maximally effective stimulant of acid secretion that was below the lower limit of normal for 365 consecutive healthy subjects. In these healthy subjects, average basal pH was 2.16 +/- 0.09 in men and 2.79 +/- 0.18 in women. In 109 consecutive experiments in 28 subjects with true hypochlorhydria, fasting gastric pH averaged 7.44 +/- 0.11 in men and 7.65 +/- 0.33 in women. Fasting pH exceeded the upper 95% confidence limit of normal (5.09 in men and 6.81 in women) in 102 of the 109 experiments (94%). Thus, fasting pH measurement was a sensitive method for diagnosing bona fide hypochlorhydria.

Gastric acid inhibitory action of a GABA-related compound, 3-amino-3-phenylpropionic acid, in the rat

The acid inhibitory properties of 3-amino-3-phenylpropionic acid, a structural GABA analogue, were studied in the perfused rat stomach preparation. 3-Amino-3-phenylpropionic acid, 10 and 30 mg/kg i.v., dose dependently supressed the gastric acid secretion induced by baclofen (2 mg/kg s.c.). This secretagogue action had been shown to be unaffected by either GABA A or GABA B receptor antagonists. The i.v. administration of 3-amino-3-phenylpropionic acid (3 and 10 mg/kg) was also effective to abolish the acid stimulatory effects of muscimol (1 mg/kg i.v.) and 2-deoxy-D-glucose (200 mg/kg i.v.). 3-Amino-3-phenylpropionic acid, even at the high dose (30 mg/kg i.v.) had no influence on the acid output in response to histamine and bethanechol. Furthermore, 3-amino-3-phenylpropionic acid had no significant effect on the acid secretion induced by electrical vagal stimulation. These results indicate that the antisecretory effect of 3-amino-phenylpropionic acid is different from those of antimuscarinics, H 2-receptor antagonists and vagal blockade. Together, the results suggest that 3-amino-3-phenylpropionic acid might act in the brain to inhibit central regulation mechanisms of gastric acid secretion, probably through GABA mechanisms.

Telenzepine, a New M1-Receptor Antagonist, Is a More Potent Inhibitor of Pentagastrin-Stimulated Gastric Acid Output Than Pirenzepine in Dogs

In conscious dogs with a gastric fistula we compared the action of different doses of telenzepine (ranging from 1 to 243 nmol/kg/h) and pirenzepine (ranging from 4.7 to 1170 nmol/kg/h) on gastric acid output in response to pentagastrin (1 to 8 micrograms/kg/h). Pentagastrin caused a dose-dependent increase in gastric acid output. A dose of 27 nmol/kg/h and all subsequent doses of telenzepine and a dose of 130 nmol/kg/h and all higher doses of pirenzepine significantly inhibited (up to 74% of control values) the gastric acid response to pentagastrin. Doses above 27 nmol/kg/h of telenzepine and doses above 130 nmol/kg/h of pirenzepine did not further inhibit the gastric acid output. Only the highest doses of telenzepine (243 nmol/kg/h) and pirenzepine (1170 nmol/kg/h) significantly increased heart rate from 66 +/- 3.1 to 77.1 +/- 3.9 and 72.5 +/- 3.2, respectively (beats/min, chi +/- SEM, n = 6). Differences between both drugs were not found with regard to cardiovascular responses of equipotent doses. We conclude that in conscious dogs with an intact stomach, the new M1-receptor antagonist telenzepine is, on a molar basis, more than 4.7 times more potent than pirenzepine in inhibiting pentagastrin-stimulated gastric acid output. This inhibition occurs at doses that do not increase heart rate, and, therefore, probably cause few systemic effects.

胃出血連続測定による実験的急性胃粘膜病変の計量的評価とエルカトニンの作用

Intraperitoneal injection of indomethacin (5, 10 and 20 mg/kg) caused acute gastric mucosal lesions in the conscious restrained rat and also hypersecretion of gastric acid. Cimetidine, an H2-receptor antagonist, was found to prevent gastric mucosal bleeding and acid secretion induced by indomethacin. Elcatonin at higher doses than 2.5 U/kg (0.5 microgram/kg) was effective for protecting the gastric mucosa against indomethacin irritation, and it inhibited acid output in response to this ulcerogen. The acid inhibitory effect of elcatonin might be implicated in its cytoprotective action.

Effects of intramural division of gastric vagal fibers on stimulated acid production

Transmural proximal gastric vagotomy, an experimental procedure designed to denervate the gastric fundus by intramural division of vagal fibers, was evaluated as a means of reducing stimulated gastric acid output. The procedure reduced peak acid output in response to insulin stimulation by 71 percent. Acid production was not further decreased by extramural division of vagal fibers. It also decreased parietal cell sensitivity to pentagastrin stimulation and did not interfere with emptying of a liquid meal. We have concluded that transmural proximal gastric vagotomy is technically straightforward, reliably divides fundic vagal fibers, produces a significant reduction in acid production equivalent to that produced by standard operative techniques, and does not interfere with gastric emptying.

Gastric acid and pancreatic polypeptide responses to modified sham feeding. Effects of truncal and parietal cell vagotomy.

The effects of truncal vagotomy and parietal cell vagotomy on gastric acid secretion and plasma gastrin and pancreatic polypeptide release were studied in 28 duodenal ulcer patients under basal conditions and after modified sham feeding and infusion of pentagastrin (2 micrograms/kg/h). Before vagotomy gastric acid output in response to modified sham feeding was significantly higher than basal acid secretion in all subjects tested and reached about 45% of the pentagastrin maximum. No difference in the increase in acid response, or in the pancreatic polypeptide response to modified sham feeding was found between patients with high and low basal secretion. Plasma gastrin concentration was unaltered by modified sham feeding before and after truncal vagotomy or parietal cell vagotomy, although after vagotomy it tended to reach higher values than before this procedure. After truncal vagotomy, basal pancreatic polypeptide concentration was decreased and modified sham feeding-induced pancreatic polypeptide increment was completely eliminated. Four weeks after parietal cell vagotomy, the modified sham feeding-induced increment in plasma pancreatic polypeptide was significantly decreased and observed only in seven of 12 patients. Four to five years after parietal cell vagotomy all subjects responded to modified sham feeding with pancreatic polypeptide increment similar to that before vagotomy and in three of 12 patients acid response to modified sham feeding was seen. This study indicates that truncal vagotomy eliminates gastric acid and plasma pancreatic polypeptide responses to vagal excitation while parietal cell vagotomy abolishes gastric acid response and reduces temporarily the pancreatic polypeptide response to modified sham feeding (possibly because of transient impairment of the vagal innervation of the pancreas). (2) A high ratio of basal to maximal acid output in non-operated duodenal ulcer patients is not associated with a low acid response to modified sham feeding, nor with a high pancreatic polypeptide concentration, and (3) Restitution of the pancreatic polypeptide response to modified sham feeding five years after parietal cell vagotomy does not indication ineffective denervation of the parietal cells.

Augmented postprandial gastric acid secretion due to exposure to ranitidine in healthy subjects.

In 10 healthy volunteers gastric acid output in response to a meal was significantly increased 60-64 h after cessation of 4 weeks of ranitidine treatment as compared with the response before treatment. Four to 6 weeks after discontinuation of treatment the acid secretory response to the meal had returned to values not significantly different from those seen before treatment. There was no change in pepsin output owing to ranitidine treatment.