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Biomedical subjects

J Vatier

Publications and source records attributed to J Vatier.

At least 73 records · Page 4Linked to original sources
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↗
PubMed1982

Effect of pirenzepine on meal-stimulated acid secretion and gastrin release in normal man.

The effect of increasing doses of pirenzepine, a tricyclic compound and new antiulcer drug, on meal-induced gastric acid secretion, gastrin release and gastric emptying of the liquid meal, was investigated in eight healthy volunteers. Gastric acid secretion was assessed using intragastric titration technique. Intra-muscularly administered doses of pirenzepine tested were 0 (placebo), 0.1, 0.25 and 0.5 mg.kg-1. With increasing doses of pirenzepine a dose-related reduction of meal-stimulated acid response was noticed amounting to 53% of control values with the highest dosage. The IC 50 value is close to 200 ng.ml-1. Initial but not total gastric emptying of the liquid protein-meal was slowed by 0.5 mg.kg-1 pirenzepine dose. Gastrin responses to the meal were reduced in a dose dependent manner although to a lesser degree.

Adult↗
PubMed1982

The gastric antisecretory activity of a phenothiazine molecule, LM 24056.

The effect on the gastric secretion of the phenothiazine molecule N,N-dimethyl-10-(3-quinuclidinyl)-2-phenothiazine sulfonamide (LM24056) was studied in dogs equipped with gastric fistula and denervated pouch. The gastric stimulation was obtained either by exogenous stimulants (gastrin, gastrin + bethanechol, histamine) or by endogenous ones released by feeding gastrin; LM 24056 was infused i.v. 1. I.v. administration of 1.25 to 5 mg . kg-1 . h-1 of LM 24056 had a nearly complete inhibitory action on gastric juice secretion (acid and pepsin), on gastrin- and gastrin + bethanechol-stimulated secretion. The LM, 24056 concentration which produced 50% inhibition (IC50%) of acid and pepsin secretion was about 1.25 mg . kg-1 . h-1. 2. LM 24056 appeared to be unable to reduce the histamine-stimulated secretion. 3. I.v. administration of 1 to 30 mg . h-1 of LM 24056 reduced or abolished both gastric acid secretion and gastrin release. The IC50 was 5 mg . h-1 (or about 0.5 mg . kg-1 . h-1) for both responses. The possible mechanism of action of LM 24056 is discussed in comparison with those of H2-receptor antagonists, of atropine and of pirenzepine, respectively.

Animals↗
PubMed1978

Parietal cell vagotomy in dogs. A comparative study of the effects on gastric secretion and antral muscle contraction.

The aim of this work was to further investigate whether it is possible, through parietal cell vagotomy (PCV), to obtain both a complete suppression of the gastric secretory response to vagal impulses and to retain a normal contractile response of the antral muscle. Acid and peptic secretions, the electrical activity and the force of circular antral contractions were simultaneously studied in dogs, before and after PCV, under 2-deoxy-D-glucose (2DG) and pentagastrin (PG) stimulation. After PCV, the response to 200 mg/kg 2DG was reduced by about 70% for acid and 80% for pepsin; the slopes of the dose-response curves were significantly reduced after PCV. The slope of the regression line pepsin/acid after 2DG was decreased following PCV. The mean acid response to PG was reduced about 50% after PCV. Plasma immunoreactive gastrin increased following 2DG, and the variations were identical before and after PCV. The gastric control electrical activity in basal conditions (fasted dogs) and following 2DG was similar before and after PCV. The antral contractile response to 2DG was reduced by about 40% after PCV. In conclusion, when PCV induced an 80% reduction in the gastric secretory response to maximal vagal stimulation by 2DG, the contractile antral response was not entirely normal. This effect might be due either to a partial antral denervation or to some intrinsic influence of the denervated gastric body upon the strength of antral contractions.

Animals↗