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At least 847 records · Page 47Linked to original sources
PubMed1988

Effect of pentobarbital on gastric acid secretion elicited by secretagogues or electrical vagal stimulation in rats under urethane anesthesia.

The effect of pentobarbital, which stimulates gastric acid secretion in urethane-anesthetized rats, on secretagogue-stimulated or electrically stimulated acid secretion was studied in the rat perfused stomach. 2-Deoxy-D-glucose (2-DG)-stimulated gastric acid secretion was markedly depressed by intravenous injection of pentobarbital, but was definitely increased by lateral cerebroventricular injection and was unaffected by injection into the fourth cerebroventricle. Bethanechol-stimulated secretion was augmented by intravenous injection of pentobarbital. In vagotomized rats, pentobarbital did not affect the bethanechol-stimulated or electrically vagally stimulated secretion. These findings indicate that pentobarbital produces both stimulatory and inhibitory effects on gastric acid secretion through a central mechanism, especially in the forebrain. It was proposed that the inhibitory response would result from some interaction of intravenous 2-DG and pentobarbital in the central regulatory system of gastric secretion.

Animals↗
PubMed1983

Augmentation of bethanechol-stimulated gastric secretion by lowering body temperature in water-immersed rats.

The present study was designed to elucidate influences of hypothermia on gastric secretory response to secretagogues (bethanechol, histamine and tetragastrin) in rats exposed to restraint plus water immersion (36 and 25 degrees C) stress. In vagotomized rats provided with a pH microelectrode, decrease in intragastric pH by bethanechol (75 micrograms/kg, i.p.) was markedly produced under the water-immersion at 25 degrees C and the extent of the pH decrease was significantly greater than that observed under the water-immersion at 36 degrees C. However, intragastric pH decrease by histamine (1 mg/kg, i.v.) or tetragastrin (60 micrograms/kg/20 min, i.v.) was not affected by varying water temperatures. Using a technique of pyloric ligation, gastric acid and pepsin responses to bethanechol were measured at doses of 50-100 micrograms/kg in vagotomized rats and also at doses of 0.5-1.0 mg/kg in vagally intact rats. Stimulation of acid and pepsin secretion by bethanechol was provoked only under the water-immersion at 25 degrees C. As compared with the values obtained under the water-immersion at 36 degrees C, a significant augmentation of bethanechol-stimulated secretion was seen for acid and pepsin output in vagotomized rats and seen for acid output in vagally intact rats under the water-immersion at 25 degrees C. These results suggest that hypothermia may operate some mechanism for increasing the secretory responsiveness of the stomach to cholinomimetics.

Animals↗
PubMed1984

Effects of brovincamine on the autonomic nervous function in the dog and rat.

Effects of brovincamine (BV) on peripheral nerves were studied in dogs and rats. 1) In pentobarbital-anesthetized dogs, BV (6.4 mg/kg) administered i.v. did not affect the changes of blood pressure and heart rate induced by noradrenaline and adrenaline, but slightly inhibited the hypotensive effect of acetylcholine. BV had no effect on the hypertension elicited by carotid sinus reflex, but diminished the bradycardia by vagus nerve stimulation. BV did not influence the tachycardia elicited by stimulation of the postganglionic nerve to stellate ganglion, but slightly inhibited that by the preganglionic stimulation. 2) In spinal dogs, BV (6.4 mg/kg) given i.v. slightly inhibited the increases of blood pressure and heart rate induced by i.v. dimethylphenylpiperazinium (DMPP). When i.v. administered in divided doses of 2 and 4 mg/kg, BV induced a slight but stepwise inhibition of the tachycardia elicited by direct administration of DMPP, bethanechol (BCH) and angiotension II (AT II) to the cardiac sympathetic ganglia via the subclavian artery. 3) In rat isolated diaphragm nerve preparations, BV at 10(-5) and 10(-4) g/ml dose-dependently reduced the twitch response to nerve stimulation. 4) In conclusion, BV does not affect the sympathetic activities but inhibits the cholinergic function in the autonomic nervous system.

Acetylcholine↗
PubMed1978

[Pharmacological actions of timepidium bromide on the motility of visceral smooth muscles and the secretion of digestive juice in experimental animals (author's transl)].

Effects of timepidium bromide (TB) on the motility of various smooth muscles and the secretion of digestive juice were examined and the activity was compared with those of hyoscine-N-butylbromide (HB) and atropine sulfate (Atr). In dogs, TB inhibited the spontaneous and bethanechol-induced motility of various regions of the gastrointestinal tract, the activity being almost the same as that of Atr but stronger than that of HB. All these drugs exhibited a similar inhibitory effect on the motility of the gallbladder. On the contrary, the inhbitory effect of TB on the spontaneous motion of urinary bladder was somewhat weaker than those of HB and Atr, while this effect on the bethanechol-induced motility was nearly equal the effects of HB and Atr. It was also evident that TB inhibited the gastric acid secretion induced by bethanechol: the activity was stronger than that of HB, while it was weaker than that of Atr. Similar effects on the gastric acid secretion were also found in rats. In the case of salivary secretion, however, TB and HB produced much weaker inhibitory actions than Atr. TB even at a higher dose produced little significant effect on the pancreatic and biliary secretion of rats. The uterine contraction induced by methacholine was inhibited by all these drugs. The mydriatic activity of TB in mice was found to be the weakest among the drugs tested.

Animals↗
PubMed1985

[Effects of somatostatin and its analog on gastric secretion. An application of the secretagogues to gastric secretion].

A simple technique to examine the effects of drugs on the gastric secretion response to the secretagogues without anesthesia was shown in this paper. The administration of bethanechol (1 mg/kg, s.c.), histamine (15 mg/kg, s.c.) or pentagastrin (0.25 mg/kg, i.p.) significantly increased the gastric volume and the total acid output in the pylorus-ligated rat. These responses to the secretagogues were inhibited by N-butylscopolamine, urogastrone or cimetidine dose-dependently. N-butylscopolamine (0.5 mg/kg, i.p.) inhibited the response to bethanechol but not that to pentagastrin or histamine. Cimetidine (5 mg/kg, i.p.) inhibited not only the response to histamine but also the acid response to bethanechol or pentagastrin. Urogastrone (5 mg/kg, i.p.) inhibited the response to these three secretagogues. The ratio of the total acid output to the gastric volume was also examined in each of the cases. Somatostatin (0.1 mg/kg, i.p.) inhibited the response to pentagastrin, but not that to bethanechol or histamine. On the other hand, an analogue of somatostatin (SS-1; 0.1 mg/kg, i.p.) inhibited the response to bethanechol but not that to pentagastrin or histamine.

Animals↗
PubMed1978

Antisecretory effect of imidazole and its derivatives in an isolated gastric mucosa preparation and an anesthetized young chicken preparation; comparison with a histamine H2-receptor antagonist.

We invesigated the influences of imidazole on the basal and the secretagogue-stimulated gastric acid secretion in isolated bullfrog gastric mucosa preparations and in anesthetized young chickens. Imidazoles (1 x 10(-4) g/ml) readily depressed the basal acid secretion in gastric mucosa in vitro. The inhibitory effect of imidazole was diminished considerably after washing out of the drug. The maximum acid secretion elicited by tetragastrin or bethanechol was completely antagonized by imidazole (1 x 10(-4) g/ml). The stimulatory action of histamine or dibutyryl cyclic AMP was also remarkably depressed in the presence of imidazole (3 x 10(-4) g/ml). after dibenamine pretreatment (5 x 10(-5) g/ml) for 60 min, the isolated gastric mucosa preparation became refractory to tetragastrin, bethanechol and histamine, but responded to dibutyryl cyclic AMP. Imidazole protected the histamine sensitivity against dibenamine blockade in the concentration of 5 x 10(-4) g/ml. In anesthetized young chickens, imidazole (200 mg/kg, s.c.) depressed tetragastrin- and histamine-stimulated gastric acid secretion. The effects of the imidazole derivatives and several antagonists (metiamide, atropine, diphenhydramine, acetazolamide and 2,4-dinitrophenol) on acid production were compared with that of imidazole. From these results, it is concluded that imidazole has a potent antisecretory effect on the basal and the secretagogue-stimulated acid secretion.

Animals↗
PubMed1979

In vivo direct effects of cholinergic agents on the inferior mesenteric and cardiac ganglia with relation to their receptors in the dog.

The relative contribution of nicotinic and muscarinic receptors to the cholinergic transmission of the inferior mesenteric ganglion was studied in spinal dogs by recording changes in perfusion pressure of the inferior mesenteric artery as an indicator of ganglionic function. Preganglionic stimulation elicited a frequency (2.5--320 Hz)-dependent rise in the perfusion pressure, which was inhibited by i.v. hexamethonium (C6) (10 mg/kg) or atropine (0.1 mg/kg) administered after C6. Acetylcholine (ACh) (0.1--1000 microgram) administered into the inferior mesenteric artery to reach the mesenteric ganglion induced a dose-dependent rise in perfusion pressure and this dose-response curve was shifted to the right by C6 or atropine. Bethanechol (1--1000 microgram) i.a. produced a dose-dependent rise in the pressure, which was abolished after i.v. atropine. Tetramethylammonium (1--300 microgram) i.a. elicited an increase in the pressure thought the effects were decreased at larger doses, and these effects were strongly inhibited by i.v. C6. ACh (5--100 microgram) administered into the right subclavian artery to reach the cardiac sympathetic ganglia caused a dose-dependent positive chronotropic effect, which was inhibited by i.a. C6 or atropine. The results suggest that the inferior mesenteric ganglion seems to differ from the cardiac ganglia in relative contribution of nicotinic and muscarinic receptors to the cholinergic transmission.

Acetylcholine↗
PubMed1983

Effect of trimebutine maleate on bethanechol-induced contractions of gastrointestinal tract in conscious and anaesthetized dogs.

The effect of trimebutine maleate (TM-906) on bethanechol-induced contractions of the gastrointestinal tract in dogs was studied by means of chronically implanted force transducers, and it was compared with that of metoclopramide and atropine. During the period of motor quiescence in the fasted state of conscious dog, a bolus i.v. injection of 10 to 50 micrograms/kg bethanechol caused rhythmic contractions in the stomach and small intestine, in which an increase in basal tone was often accompanied in the distal ileum. The stomach responded to a less extent than the small intestine. Intravenous infusion of TM-906 at 3.0 mg/kg-hr for 20 to 60 min reduced the gastric contractions induced by 20 to 30 micrograms/kg bethanechol in five out of six conscious animals examined. The drug, however, enhanced the contractions of the duodenum and jejunum in a majority of the animals. Metoclopramide (1.8 mg/kg-hr) showed a tendency to potentiate the bethanechol-induced contractions in the stomach and small intestine, and atropine (0.06 mg/kg-hr) diminished them. In pentobarbital-Na anaesthetized dogs, effects of TM-906 on bethanechol-induced contractions resembled those in conscious dogs, inhibition in the stomach and potentiation in the small intestine.

Animals↗
PubMed1986

Some profiles of transmucosal potential difference in rat stomach determined in situ with special reference to effects of timoprazole, a H+,K+-ATPase inhibitor.

Gastric transmucosal potential difference (PD) is referred to an index of function and integrity of the mucosa. The features of gastric PD were studied in association with gastric acid secretion. The gastric PD was measured at the forestomach, glandular portion and pylorus in the rat in in situ preparations. Secretagogues such as bethanechol (BeCh, 50 micrograms/kg, i.v.), tetragastrin (TG, 30 micrograms/kg, i.v.), and histamine (Hist, 10 mg/kg, s.c.) produced a decrease in PD at the three regions of the stomach. These PD reductions did not occur with the combined treatment with timoprazole (30 mg/kg, i.d.); a marked increase in PD was noted, especially, in the case of Hist plus timoprazole. Similarly, BeCh induced PD decrease was antagonized by atropine (30 micrograms/kg, i.v.) and Hist induced PD decrease was attenuated by cimetidine (10 mg/kg, i.v.), while TG induced PD decrease was not affected by either of them. Of the antisecretory drugs, only cimetidine produced an increase in basal PD, probably via a mechanism unrelated to acid secretion. These results suggest that the PD decrease by each secretagogue seen at oxyntic and non-oxyntic gland regions of the stomach primarily originates from secretory activation of the parietal cells and that its action on function unrelated to acid secretion also exerts a minor influence on gastric PD.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1987

Parasympathetic denervation supersensitivity in the rat iris sphincter muscle: an in vitro study.

Supersensitivity in chronically sympathectomized smooth muscle has long been studied, but little is known about chronically parasympathectomized smooth muscles. Iris is one of the few smooth muscle organs which can be parasympathetically denervated. We used rats because the denervation supersensitivity in the vas deferens has extensively been studied in this species. The rat was unilaterally ciliary-ganglionectomized. After 1-13 days, strips of the iris sphincter muscle obtained from denervated eye were tested for the sensitivity to acetylcholine (ACh), 5-hydroxytryptamine (5-HT) and K+. A significant increase in sensitivity to ACh and 5-HT was recognized as early as 1 day after the operation, and the sensitivity reached a maximum after 5-6 days, when ED50 values of ACh and 5-HT were reduced to approximately 1/28 and 1/4, respectively. The sensitivity to K+ was unaffected. When the sensitivity reached the maximum, the maximum responses to ACh, 5-HT and K+ were increased by 50%, 140% and 50%, respectively. The shift of the dose-response curve for bethanechol (BeCh) after denervation was comparable to that for ACh. Physostigmine shifted the curve for ACh, but did not shift that for BeCh either before or after denervation. Specific binding of 3H-quinuclidinyl benzylate tended to decrease after denervation, but the change was statistically not significant. These results indicate that the parasympathetic denervation supersensitivity in the rat iris sphincter involves a non-specific component, in addition to one specific to ACh and BeCh. The specific component seems to involve postsynaptic mechanisms.

Acetylcholine↗
PubMed1987

Inhibitory effect of somatostatin on gastric acid secretion in rats.

Effects of somatostatin on parasympathetically induced increases in gastric acid secretion and mucosal blood flow (MBF) were studied in anesthetized rats with a gastric fistula. Intravenous infusion of small doses of somatostatin (0.1-0.5 microgram/kg/min) dose-dependently inhibited the increases in the vagally stimulated gastric acid secretion. Larger doses of somatostatin (0.5-2.5 micrograms/kg/min) also dose-dependently inhibited the bethanechol-induced gastric acid secretion. The dose of somatostatin required to inhibit the gastric acid secretion by about 50% of the preinfused control values was 0.25 microgram/kg/min for vagally stimulated acid secretion and 2.5 micrograms/kg/min for bethanechol-induced acid secretion. Thus, the inhibitory potency of somatostatin on the vagally stimulated gastric acid secretion was about 10-fold higher than that on bethanechol-induced acid secretion. Somatostatin had no effect on the increase in gastric MBF during vagus nerve stimulation or bethanechol infusion. Pretreatment with indomethacin or phentolamine had no effect on the inhibitory effect of somatostatin on the increase in gastric acid secretion during vagus nerve stimulation or bethanechol infusion. These results suggest that somatostatin exerts an inhibitory effect on gastric acid secretion by acting on the parasympathetic neurons in the gastric wall more than on the structures peripheral to the parasympathetic nerve terminals, and it reduces parasympathetically stimulated gastric acid secretion in rats. This inhibitory effect of somatostatin on the gastric acid secretion is independent of the changes in the gastric MBF and probably not related to prostaglandin-involved or alpha adrenoceptor-mediated mechanisms.

Animals↗