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Biomedical subjects

S Bonfils

Publications and source records attributed to S Bonfils.

At least 91 records · Page 5Linked to original sources
PubMed1984

Gastric acid secretion results from antagonistic effects of antral histamine (Antramine) and somatostatin on gastrin.

Gastric acid secretion, whole blood histamine concentration and serum gastrin were measured in dogs, equipped with Heidenhain pouch, in response to feeding alone and in combination with antral histamine (AH)--Antramine--or with somatostatin. Feeding stimulated acid secretion, histamine and gastrin responses in a dose-related manner. Addition of antramine to feeding resulted in a potentiated acid and gastrin responses while histamine response corresponded to sum of individual responses to antramine and to feeding. Somatostatin reduced markedly acid and histamine responses, while gastrin response was unchanged. Serum gastrin and whole blood histamine appear to be agonistic factors responsible together for acid secretion. Somatostatin suppresses histamine response and would inhibit gastrin activity on acid secreting cells by this mean. Somatostatin and histamine might act antagonistically on gastrin which would be their common substrate, and thus they could intervene in a regulation process of acid secretion. In regard to synthetic histamine, native antral histamine--antramine--appears to be a better candidate for a physiological histamine regulation of acid secretion.

Animals↗
PubMed1984

Consecutive phases of gastric acid response to secretin in rats with chronic hypergastrinemia.

Secretin is known to inhibit gastric acid secretion but in some cases is able to stimulate both gastrin release and acid output. Different studies suggest that gastrin concentration at the parietal cell level modulates the acid response to secretin. Our purpose was to investigate in rats with chronic endogenous hypergastrinemia, as well as in control rats, the effect of an intravenous bolus of secretin GIH (from 0.25 to 4 clinical units (CU)/rat) on acid secretion. Both groups of rats were equipped with a chronic double gastric fistula allowing the collection of diluted gastric secretion every 2 min. We observed a dose-related inhibition of acid output (ID 50 less than 0.5 CU/rat) by secretin. In addition, in rats with hypergastrinemia; the acid response was phasic: an initial increase of acid output forewent its inhibition by 4 CU secretin. This phasic response suggests that secretin could act on acid secretion by releasing mediators which stimulate (as gastrin) and/or inhibit (as somatostatin) acid output.

Animals↗
PubMed1984

[Influence of ranitidine during a 24-hour period on the level of nitrites, nitrates, nitrosamines and bacterial flora in the gastric juice of healthy subjects].

The aim of this study was to determine the influence of 24 h of ranitidine treatment on gastric bacterial flora and N-nitroso compound formation. Nitrate, nitrite levels, N-nitroso compound concentration were measured and bacterial flora was studied in the fasting and postprandial gastric juice of four healthy men under placebo and ranitidine treatment (150 mg. bid). The pH of seventy-five per cent of the gastric juice samples was over 4 when the patients received their ranitidine treatment. While the mean intragastric concentrations of nitrate, nitrite, N-nitroso compounds and counts of nitrate-reducing organisms were not significantly altered by ranitidine, there was a statistically significant rise in the number of total bacteria. During ranitidine treatment, the nitrite/nitrate ratio was positively correlated with intragastric pH and with the nitrate-reducing organism count of the placebo period. These results suggest that the reduction of nitrate to nitrite required the combination of two factors: a high count of nitrate-reducing organisms before treatment and a high intragastric pH.

Adult↗
PubMed1984

[Zollinger-Ellison syndrome. Therapeutic aspects].

This review considers the place of surgery with its two indications: 1) suppression of the target organ of gastrin hypersecretion (total gastrectomy or other surgical procedures on the stomach), 2) radical tumour excision. The authors also discuss the use of anti-secretory drugs currently used in the Zollinger-Ellison syndrome and the respective usefulness of these different techniques in acute and chronic Zollinger-Ellison syndromes. The role of anti-tumour chemotherapy is also discussed.

Cimetidine↗
PubMed1984

[Gastric secretory, ultrastructural and pH changes during prolonged treatment with omeprazole in a severe form of Zollinger-Ellison syndrome].

Omeprazole, a powerful and long-lasting gastric anti-secretory benziimidazole derivative has been used to treat a particularly severe case of Zollinger-Ellison syndrome with familial type I multiple endocrine involvement. Before treatment with omeprazole, the patient's basal acid secretion, ranging from 50 to 100 mmol/h, had been poorly controlled by cimetidine (doses of up to 2,400 mg/d), ranitidine (doses of up to 1,200 mg/d) and even by ranitidine (1,200 mg/d) combined with pirenzepine (150 mg/d). Upon oral administration of four 20-mg capsules of omeprazole twice daily, rapid healing of the diffuse mucosal ulcerations of the upper GI tract as well as control of diarrhea were achieved. Clinical benefit accompagnied dramatic and sustained reductions in gastric acid secretion as demonstrated by repeated basal output measurements and 24-hour intragastric pH recording. The biodisponibility of omeprazole improved as gastric intraluminal acidity was reduced. The effects of omeprazole on pepsin output appeared to be mainly related to the reduction of gastric secretory volume. After more than one year of treatment, neither clinical nor biological side-effects were noted. However, repeated ultrastructural studies of fundic gastric mucosa revealed two types of alterations: a) a pattern of hyper-stimulated parietal cells with turgescent intra-cellular micro-canalicus invested by numerous microvilli; b) in about a fourth of the parietal cells, cytoplasmic modifications resembling auto-phagosomia and mitochondrial reduction in number and morphological transformation. Poorly understood to date, these alterations call for regular histological control of the gastric mucosa in patients with Zollinger-Ellison syndrome submitted to long-term administration of large doses of omeprazole.

Adult↗
PubMed1984

[Efficacy of a new antisecretory agent (40 749 RP) on human gastric secretion induced by a meal (intragastric titration)].

An antisecretory drug of a new series, 40 749 RP, without anticholinergic or H2 receptor antagonist activities, was tested on meal-induced gastric acid secretion in 6 healthy volunteers. Gastric acid secretion and emptying of liquid were measured using intragastric titration. Oral dosages tested were 1, 2 and 4 mg/kg versus placebo. Inhibitions obtained were dose-related and expressed in percentage of the placebo values: 36 +/- 10 p. 100 for 1 mg/kg; 51 +/- 13 p. 100 for 2 mg/kg and 83 +/- 5 p. 100 for 4 mg/kg. Statistically significant correlation (p less than 0.001) was observed between maximal blood concentration of 40 749 RP and the percentage of secretory inhibition during the 90 min of the test. No change in gastrin response or in gastric emptying was observed whatever the dose.

Adult↗
PubMed1983

Determination of histamine, methylhistamines and histamine-o-phthaldialdehyde complexes by two high-performance liquid chromatographic procedures. Application to biological samples.

Two high-performance liquid chromatographic procedures were proposed to measure histamine. The first, with UV detection and a strong acid cation exchanger (Partisil 10, SCX Whatman), made it possible to isolate histamine and some methylated derivatives. The second, with a C18 sorbent (mu Bondapak, Waters, 10 microns particle size) eluted with ion-pairing phases, made it possible to isolate the histamine-o-phthaldialdehyde complexes. This last procedure allied with a chromatographic purification step gave lower or identical amounts of histamine than those described in human urine (16 +/- 7 micrograms per 24 h), canine whole blood (1.5 +/- 1 ng/ml) and human gastric juice (2.3 +/- 1.4 ng/ml). The two procedures gave the concentration of a histamine-like compound isolated from the antral mucosa.

Animals↗
PubMed1983

Evaluation of antisecretory drug therapy of Zollinger-Ellison syndrome (ZES) using 24-hour pH monitoring.

Clinical and endoscopic findings were compared with 24-hr pH profiles in 8 patients with Zollinger-Ellison syndrome (ZES), who were being treated, during consecutive periods, with doses of cimetidine or ranitidine. There was a positive correlation between the effect on gastric pH and the outcome of treatment, with ranitidine proving to be more effective. The reduction of gastric acidity was correlated with ranitidine plasma levels. In the medical management of ZES patients, the 24-hr pH profile appears to be a measurement which is of value in the choice of appropriate drug regimes and which promises to increase our understanding of treatment failure.

Adult↗
PubMed1983

Histamine is able to suppress the inhibitory effect of somatostatin on exogenous gastrin: comparison between extractive antral histamine and synthetic histamine.

In view of examining inhibition by somatostatin of gastrin-induced gastric secretion, antral histamine (AH) and synthetic histamine (SH) were comparatively studied in dogs. Both AH and SH were able to antagonize somatostatin: their potencies did not differ significantly as regards acid secretion, but AH is more potent than SH on pepsin secretion. The dose-dependent activity of AH was limited for the period of infusion. The denervated pouch is more sensitive than the innervated stomach. We suggest that antral histamine might intervene in the complex regulation of gastric secretion where somatostatin and gastrin act antagonistically and where the stimulatory as well as inhibitory fibers of the vagus intervene.

Animals↗
PubMed1983

N,N-dimethyl-10-(3-quinuclidinyl)-2-phenothiazine sulfonamide (LM 24056): mode of action of its gastric antisecretory effect.

The inhibitory effect on gastric secretion of a phenothiazine molecule, N,N-dimethyl-10-(3-quinuclidinyl)-2-phenothiazine sulfonamide (LM 24056), was studied in dogs equipped with gastric fistula (GF) and Heidenhain denervated pouch (HP). LM 24056 was infused intravenously before exogenous stimulations started: the gastric stimulation ws obtained either by gastrin, by combination of gastrin + bethanechol (subthreshold dose) or by histamine. 1. On gastrin-stimulated secretion, preliminary infusion of LM 24056 results in a weak and non-significant reduction on GF acid secretion, while on HP, the inhibition is significant with 1 and 2 micrograms x kg-1 x h-1 of gastrin. The LM 24056 concentrations which produced 50% inhibition (IC50) of acid secretion is close to 0.5 mg x min-1. 2. LM 24056 exerts a strong inhibitory effect on combination gastrin + bethanechol-stimulated acid and pepsin secretions on GH and HP. IC50 is close to 0.25 mg x min-1. 3. LM 24056 is able to delay the histamine-stimulated acid secretion. There are some differences in the gastric inhibitory effects in relation to the moment of LM 24056 administration regarding exogenous stimulant: LM 24056 seems to be able to compete gastrin and to delay the normal histamine stimulation. The most important inhibitory effect is exerted on combination gastrin + bethanechol. LM 24056 could act as an antigastrinic substance.

Animals↗
PubMed1983

[Role of antral histamine and gastrin in gastric acid secretion: experimental facts and hypotheses].

Histamine isolated from the gastric antral mucosa probably potentiates the secretory activity of gastrin by suppression of the inhibitory effect of somatostatin on gastrin. In dogs with gastric fistula and Heindenhain pouch, acid secretion was obtained in response to exogenous gastrin, antral histamine or various combinations of both stimulants. Acid output was expressed by graphic representation: the administered doses of gastrin and antral histamine were reported respectively, on the X and Y axis, the acid output values were plotted on the intersection of the stimulant dosages used, and curves of equal acid outputs were drawn. This representation was used to approach the physiological and physiopathological mechanisms of gastric secretion, considering that gastrin and antral histamine could be the main parameters. It also seems possible that an histaminic factor could be involved in secretion processes. Excess or lack of one of the other stimulants could be responsible for an increased or a decreased secretory response: these facts can be related to the curves of high acid output or low acid output observed in the animal. Thus, histamine, especially of antral origin, might be an important component of the secretion mechanism, by modulation of gastrin activity; both substances could be the main mediators of somatostatin-induced inhibition.

Animals↗