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PubMed1984

Effect of met-enkephalin on acid secretion from gastric fistulas and Heidenhain pouches in dogs stimulated by pentagastrin, pentagastrin plus bethanechol, or a meal.

In dogs with denervated Heidenhain pouches and gastric cannulas the authors studied the action of met-enkephalin on acid secretion stimulated by a liquid meal, pentagastrin or pentagastrin + bethanechol. Serum gastrin levels were determined during the feeding experiments. Meal-stimulated and pentagastrin-stimulated acid secretion from the gastric fistula were inhibited by met-enkephalin. A rise in pentagastrin-induced acid secretion was observed in the denervated stomach. No significant changes were observed in the postprandial acid response from the pouch to the meal, nor from the main stomach or the pouch during stimulation with pentagastrin + bethanechol. Gastrin release was decreased by met-enkephalin during the first hour following feeding and increased during the second hour. Our data indicate that met-enkephalin can either inhibit or stimulate acid secretion in dogs. The inhibition occurs only in the innervated fundic mucosa, and might be explained by a decrease in gastrin release and by a decrease in vagal tone.

Animals↗
PubMed1981

Physiological stimulation of pepsin secretion. The role of vagal innervation.

The studies were performed on eight double-pouch dogs with one vagally innervated Amdrup pouch (AP) and one denervated Heidenhain pouch (HP), allowing comparison of pepsin secretion from innervated and denervated mucosa at the same time in the same animal. Food stimulation was done with a mixture of liver, heart, and bonemeal in doses of 1.25, 2.5, 5, 10, and 20 g/kg body weight, plus maximal stimulation by repeated meals of 5 g/kg every 15 min up to 10 times. 'Non-active' secretion of pepsin was determined by instillation in the pouches of 0.1 M and 0.005 M HCl dissolved in 0.15 M NaCl. The pepsin secretion in the HP equalled the 'non-active' output for all doses of food. In the innervated pouch there was an immediate, very high pepsin output similar to the response that can be elicited by 2-deoxy-D-glucose and bethanechol chloride. The secretion of pepsin was gradually reduced, but it was, as long as the volume and electrolyte secretion lasted. well above the 'non-active' level. The results show that stimulation of pepsin secretion by food is completely dependent on intact vagal innervation. The volume and acid output were increased as the dose of food was increased, but the concentration of pepsin was stepwise reduced when the volume increased, resulting in approximately the same output of pepsin for all doses of food. The pepsin to acid ratio was statistically higher in juice secreted from innervated than from denervated mucosa for all doses of food, for lower doses of histamine and pentagastrin, and for higher doses of bethanechol chloride.

Animals↗
PubMed1981

Acid secretion in patients with Chagas' disease.

In order to evaluate the acid secretory pattern in patients with Chagas' Disease when compared to control subjects, the following tests were performed; a) Basal Secretion, b) Acid output after increasing doses of I.V. Pentagastrin (1, 2, 4 and 8 micrograms/Kg-h); c) I.V. Pentagastrin (P) plus a background of subthreshold doses of Urecholine (U) (40 micrograms/Kg-h); d) Calcium infusion test (4 mg of Ca++/Kg-h). The histological aspects of the antral and fundic mucosa was studied on 11 CD patients through samples obtained during gastroscopy. Basal, Pentagastrin stimulated acid secretion and Ca++ stimulated secretion were statistically lower in CD patients when compared to controls. Association of P + U resulted in a higher acid response in 4 out of 8 CD patients but, the mean result of the group was not statistically significant. These results suggest that the lower basal and stimulated acid response of CD patients is related to a decreased sensitivity of the parietal cell. This lower sensitivity is probably dependent on vagal blockage as a consequence of the intramural nerve destruction. The possibility of a smaller stomach and consequently small parietal cell population could not be ruled out in this investigation. However this possibility seems very unprobable to the authors.

Adolescent↗
PubMed1982

Analysis of the 2-deoxy-D-glucose-induced vagal stimulation of gastric secretion and gastrin release in dogs using methionine-enkephalin, morphine and naloxone.

Gastric acid and pepsin secreted in 3 hr and antral gastrin released in response to vagal excitation induced by 2-deoxy-D-glucose (2DG), 625 mumol/kg i.v., were studied in six conscious trained gastric fistula dogs. During a 2-hr infusion, Met-enkephalin (96 nmol/kg/hr; delta receptor) reduced the 2DG response by 50%; when the enkephalin was stopped there was a rapid rebound to peak values. Met-enkephalin also blocked the release of gastrin in the first 15 min. By itself, Met-enkephalin did not stimulate secretion and slightly depressed gastrin. By contrast, morphine (96 nmol/kg/hr; mu receptor) augmented and sustained the 2DG gastric acid secretory response. This effect was blocked by naloxone. Morphine alone caused a small rise in serum gastrin after 90 min, followed by a delayed gastric acid secretion of about 30% of the peak 2DG response. Naloxone, a mu opiate antagonist (mu/delta, 27:1), also inhibited the 2DG gastric secretory response by about 50% and augmented the Met-enkephalin inhibition of secretion without blocking either the secretory rebound or the effect on gastrin release. None of the three opiates changed the direct cholinergic gastric secretory or gastrin-releasing effects of bethanechol. Thus, vagal stimulation of the stomach involves pathways which can be influenced by both mu and delta opiates, with apparently opposite effects, proximal to the level of acetylcholine action on the gastric mucosa. The central and peripheral control points in the activation of the stomach via the vagus which are sensitive to opiates have yet to be located and explained.

Animals↗
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↗
PubMed1983

Prospective manometric evaluation with pharmacologic provocation of patients with suspected esophageal motility dysfunction.

Thirty-four consecutive patients referred to a gastroenterology clinic with suspected esophageal motility abnormality as a cause of their chest pain or dysphagia, or both, were prospectively studied in an 18-mo period. Peristaltic response to 10 wet (5 ml H2O) swallows was recorded in all studies with a low-compliance infusion system. To provoke symptoms and motility abnormalities after baseline evaluation, all patients had acid infusions (0.1 N HCl) and administration of edrophonium (80 micrograms/kg i.v.), pentagastrin (6 micrograms/kg s.c.), and bethanechol (40 micrograms/kg s.c.). Tracings were coded, read, and interpreted blindly. Baseline tracings were abnormal in 23 of 34 patients (68%), including increased amplitude peristaltic contractions ("nutcracker esophagus") in 10 and nonspecific esophageal motor disorders in 13. Acid infusion produced substernal burning in 3 of 33 patients, in motility change in 1 patient. Edrophonium produced chest pain with manometric changes in 6 of 34 (18%) patients. Pentagastrin produced chest pain with manometric change in 1 patient. Bethanechol produced chest pain with manometric change in 2 patients. One patient with low amplitude had elevation of esophageal baseline and multiple simultaneous contractions but no chest pain (subsequently developed achalasia). It was concluded that (a) abnormal motility is a common finding in a symptomatic group of patients with presumed esophageal motility disorder, (b) the "nutcracker" esophagus is the most frequent defect, and (c) attempted provocation of symptoms with acid or drugs is not generally effective; however, edrophonium is the best tolerated and most effective of currently available drugs.

Adult↗
PubMed1978

The pathophysiology and treatment of gastroesophageal reflux disease: new concepts.

In summary, the recent understanding of the pathogenesis of gastroesophageal reflux disease as owing to LES incompetence has led to improvement in both the diagnosis and the treatment of this disorder. Diagnosis now dependent on demonstrating the presence of reflux, an incompetent sphincter mechanism, or some complication of reflux. Treatment is focused on reducing the endogenous factors that contribute to reflux, or actually restoring the sphincteral barrier to reflux by pharmacologic or surgical means.

Bethanechol Compounds↗
PubMed1983

Relationship between acid secretion and blood flow in the canine stomach: role of oxygen consumption.

The relationship of acid secretion to blood flow and oxygen consumption was investigated in the isolated canine stomach during intraarterial infusion of pentagastrin. Blood flows above and below control values were achieved by pump perfusion and partial arterial occlusion, respectively. When blood flow was increased from a control value of 38 ml X min-1 X 100 g-1 to 85 ml X min-1 X 100 g-1, both acid secretion and oxygen consumption remained constant at 0.08 mEq X min-1 X 100 g-1 and 2.1 ml X min-1 X 100 g-1, respectively. A reduction in blood flow to 9.0 ml X min-1 X 100 g-1 caused acid secretion and oxygen consumption to decrease to 26% and 44% of control values, respectively. The results indicate that acid secretion is independent of blood flow at flow rates above 38 ml X min-1 X 100 g-1. A model of the interrelationships between blood flow, oxygen consumption, and acid secretion is proposed that may explain much of the conflict in the literature concerning these three parameters.

Animals↗
PubMed1983

Esophageal motility during food ingestion: a physiologic test of esophageal motor function.

It is unknown whether esophageal motility, as assessed by standard motility testing, bears close relationship to motility occurring during food ingestion. Certainly, many patients, while reporting symptoms during food ingestion, are asymptomatic during standard motility testing; thus, a direct link between abnormal motility and symptomatology is often lacking. Twelve normal subjects and 5 patients with symptomatic esophageal motility disorders, therefore, underwent motility testing during upright ingestion of a meal which consisted of beef cubes and gravy. In normals, contraction parameters during food ingestion could not have been predicted by values obtained during standard testing (r = 0.2, p greater than 0.05). All 5 patients, although asymptomatic during standard testing, reported dysphagia during food ingestion. Evidence of abnormal motility could be observed simultaneously. Patterns of abnormality included nonperistaltic contractions (7.2 +/- 2.5 episodes per meal), instances of incomplete lower esophageal sphincter relaxation (2.8 +/- 0.8 episodes per meal), and instances of lack of complete lower esophageal sphincter relaxation during ongoing esophageal contractions (4.6 +/- 1.0 episodes). These abnormalities were significantly more frequent in patients than in controls (p less than 0.001), and most had not been observed during standard testing in the patients. In addition, bethanechol significantly increased abnormal motility and increased dysphagia during food ingestion in the patients, but was without significant effect in controls. It was concluded, therefore, that recording of esophageal motility during upright food ingestion appears to be of value in the diagnosis and characterization of motor abnormalities in patients with symptoms of esophageal motor dysfunction.

Adult↗
PubMed1983

Determinants of esophageal acid clearance in normal subjects.

In this study, we evaluated factors that affect esophageal acid clearance in normal subjects. A 15-ml bolus of 0.1 N HCl (pH 1.2) was injected into the esophagus, and the subject then swallowed every 30 s. Manometric and pH monitoring demonstrated that esophageal acid clearance occurred by a series of step increases in pH, each associated with a swallow-induced peristaltic sequence. Between peristaltic sequences, pH increase was minimal. Saliva stimulation by oral lozenge greatly improved acid clearance, while oral aspiration of saliva abolished the step increases in esophageal pH and markedly delayed acid clearance. Replacement of aspirated saliva with a bicarbonate solution reproduced the step increases in esophageal pH and restored acid clearance toward normal, while replacement with water alone failed to improve acid clearance. Similar to the effect of the oral lozenge, bethanechol (5 mg subcutaneously) improved esophageal acid clearance, but this improvement was reversed by oral aspiration of saliva, which markedly delayed acid clearance. A change from the recumbent to the sitting position tended to improve acid clearance slightly, but this improvement was not statistically significant. We concluded that in normal subjects (a) swallowing carries saliva into the esophagus and peristalsis empties intraesophageal fluid into the stomach, (b) the neutralization of acid by saliva carried into the esophagus with each swallow accounts for the occurrence of acid clearance by step increases in pH, (c) the improvement in acid clearance with bethanechol is due to saliva stimulation, and (d) gravity contributes little to esophageal acid clearance in the presence of normal peristaltic stripping waves.

Adult↗
PubMed1980

Effect of nicotine on single cell activity in the noradrenergic nucleus locus coeruleus.

The effect of nicotine and various cholinergic and anticholinergic drugs on brain noradrenaline (NA) containing neurons in the locus coeruleus (LC) of the rat was studied utilizing single cell recording techniques and microiontophoretic drug application. Nicotine (10--50 micrograms/kg i.v.) caused a dose-dependent, short-lasting increase in the firing rate of NA neurons in the LC. When microiontophoretically applied nicotine had no effect on LC neurons, which in contrast were activated by acetylcholine (ACh) and the muscarinic agonist, bethanechol. The stimulation of NA neurons in the LC by i.v. physostigmine was antagonized by scopolamine but not by methylscopolamine. Also microiontophoretically applied scopolamine specifically antagonized the NA-cell activation by ACh. Consequently, nicotine probably causes an indirect activation of NA neurons in the LC. These cells seem to be equipped with excitatory, cholinergic receptors of muscarinic but not nicotinic character. The LC activating effect of nicotine may be important for its arousal producing properties.

Acetylcholine↗