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PubMed1983

Cholinergic stimulation and inhibition of pancreatic secretion in alcohol-adapted dogs.

There is indirect evidence of increased release of acetylcholine in the exocrine pancreas of chronically alcoholic dogs. Our aim was to ascertain whether altered pancreatic responsiveness to cholinergic stimulation was an associated phenomenon. Pancreatic dose-response tests with graded bethanechol stimulation on constant secretion stimulation, without or with a low dose of background atropine, were performed in four chronic gastric and duodenal fistula dogs after 3 and 12 months of intragastric feeding with ethanol. The secretory protein response was dose-dependently increased by bethanechol in the control dogs but not in the test dogs, after 3 or 12 months of daily alcohol. They responded significantly only to a dose four to eight times greater than the minimum effective dose in the control dogs. Atropine depressed the entire dose-response curve of these dogs but only the response to the greatest doses in the alcohol-treated dogs. In previous experiments caerulein and/or secretin evoked increased secretory responses of bicarbonate in chronically alcoholic dogs, but this was not the case in this study with bethanechol, which did not have a stimulating effect on bicarbonate in either test or control dogs. Concomitant atropine, however, unmasked a bicarbonate-stimulating effect of bethanechol in control but not in treated dogs. It is concluded that chronic alcohol-feeding, already after 3 months, leads to a diminished pancreatic responsiveness to cholinergic stimulation and inhibition of protein output, as evidenced by at least a fourfold increase of the minimum effective dose of bethanechol and diminished inhibitory action of atropine.

Adaptation, Physiological↗
PubMed1985

Acid secretion and mucosal blood flow in the distal and proximal parts of the canine parietal cell mass in response to cholinergic stimulation.

Dogs provided with one denervated gastric pouch in the distal part of the corpus fundus and another of equal size in the proximal part were studied during stimulation with bethanechol chloride. Dose-response curves were determined for acid output and for mucosal blood flow, which was measured with the neutral red technique. ED50 for acid output was almost identical for the two pouches, giving a value of 1.13 (median) for the ratio of ED50 proximal pouch to ED50 distal pouch, which is between the ratios of 3.54 and 0.65 noted for pentagastrin and histamine, respectively in earlier investigations. The ED50 for blood flow was significantly lower than that for the simultaneous acid output, with a value of 0.28 for the ratio of ED50 blood flow to ED50 acid output, which gives an intermediate position between the ratios for pentagastrin (0.13 and 0.21 for the distal and proximal pouch, respectively) and histamine (0.61 and 0.73) obtained in earlier investigations. It could be hypothesized that the above differences in ratio between these three agonists reflect a difference at the receptor level of the parietal cells and the arterioles.

Animals↗
PubMed1985

Exogenous serotonin and gastric mucosal blood flow in conscious dogs.

The effects of serotonin on pentagastrin- and bethanechol-stimulated gastric mucosal blood flow (GMBF) and acid secretion were evaluated. Conscious gastric fistula dogs were used, with neutral red clearance as the method to estimate the mucosal blood flow. Serotonin inhibited the acid secretion, with a counteracting effect of propranolol and methysergide. Serotonin inhibited the pentagastrin- and bethanechol-stimulated GMBF after 15 min of infusion. The ratio between GMBF and acid secretion was increased during serotonin infusion, which suggests primary and independent changes in both variables. Propranolol and methysergide counteracted the serotonin inhibition of the GMBF. It may be concluded from this study that the acid-inhibitory effect of serotonin is not mediated by changes in the GMBF. The actions of serotonin on acid secretion and GMBF are mediated by specific receptors.

Animals↗
PubMed1985

Effect of somatostatin on bethanechol-stimulated gastric pepsin secretion in gastric fistula dogs.

The effect of somatostatin on pepsin secretion was determined in six dogs with gastric fistulas during stimulation with bethanechol. Somatostatin inhibited dose-dependently the stimulated pepsin secretion, with a dose of 0.3 micrograms/kg/h being 35% inhibitory during stimulation with bethanechol, 80 micrograms/kg/h. Continuous infusion of somatostatin for 3 h did not cause any signs of tachyphylaxis. Withdrawal of somatostatin produced a return to the control level. The dose-response kinetics with five doses of bethanechol with and without somatostatin showed inhibition of a noncompetitive type. The effects of somatostatin were not altered by using adrenergic, dopaminergic, or serotonergic blocking drugs.

Adrenergic beta-Antagonists↗
PubMed1985

Effect of somatostatin on bethanechol-stimulated gastric acid secretion and gastric antral motility in dogs with gastric fistula.

The purpose of the present study was to evaluate the effect of somatostatin on gastric acid secretion and gastric antral motility in conscious dogs with gastric fistula. Infusion of bethanechol stimulated dose-dependently acid secretion, whereas the frequency and strength of antral motility was maintained at a high level. Somatostatin inhibited dose-dependently the stimulated acid secretion, whereas the effect on antral motility was more complex, acting especially on the amplitude of the contractions. The effects of somatostatin were not altered by using alpha-adrenergic, beta-adrenergic, dopaminergic, and serotonergic blocking drugs. The dose-response kinetics with four doses of bethanechol with and without somatostatin showed inhibition of a non-competitive type for gastric acid secretion and of a competitive type for antral motility with regard to amplitude.

Adrenergic alpha-Antagonists↗
PubMed1986

Effect of serotonin on bethanechol-stimulated gastric pepsin secretion in dogs.

The effect of serotonin on bethanechol-stimulated gastric pepsin secretion was evaluated with regard to dose-response kinetics and receptor mediation. A low dose of exogenous serotonin produced a stimulation (0.5 microgram/kg/min), whereas inhibition was found for higher doses (5-10 micrograms/kg/min). The inhibition was non-competitive and could be significantly counteracted by beta-adrenergic blocking drugs. This study confirms results obtained during pentagastrin stimulation and supports the concept that serotonin acts via sympathetic nerves to release noradrenaline.

Adrenergic beta-Antagonists↗
PubMed1986

Effect of serotonin on bethanechol-stimulated gastric acid secretion and gastric antral motility in dogs.

The purpose of the present study was to evaluate the effect of serotonin on bethanechol-stimulated gastric acid secretion and antral motility in conscious dogs with gastric fistula. Bethanechol stimulated the acid secretion dose-dependently and maintained the frequency and strength of the antral contractions at a high level. Serotonin inhibited the acid secretion dose-dependently, whereas the antral motility was stimulated. The acid inhibition was blocked by propranolol, and dose-response analysis showed inhibition of a non-competitive type. This study thereby shows that serotonin inhibits bethanechol-stimulated gastric acid secretion similarly to salmefamol (beta 2-adrenergic agonist)--that is, dose-dependently and non-competitively. Serotonin has been proposed to be a mediator of the beta-adrenergic influence on gastric function in vivo, but the counteracting effect of propranolol and the stimulatory effect of serotonin on motility contradict this hypothesis.

Animals↗
PubMed1986

Somatostatin increases the ratio between gastric mucosal blood flow and gastric acid and pepsin secretion in dogs.

The effects of somatostatin on gastric mucosal blood flow (GMBF), acid secretion, and pepsin secretion were evaluated. Conscious gastric fistula dogs were used, with neutral red clearance as the method for estimating the mucosal blood flow. Somatostatin inhibited the pentagastrin- and bethanechol-stimulated gastric acid and pepsin secretion and resulted in an absolute decrease in mucosal blood flow. The ratios between GMBF and secretion (acid and pepsin) were increased during somatostatin infusion, which suggests a relative increase in mucosal blood flow and independent inhibition of gastric secretion. It may be concluded from this study that the acid- and pepsin-inhibitory effects of somatostatin are not mediated by changes in the GMBF.

Animals↗
PubMed1986

Does ethanol exert its effect on the canine pancreas by mediation of cholinergic nerves?

Previous studies had shown an atropine sensitive, excitatory action of i.v. ethanol on pancreatic protein secretion in alcohol fed dogs and also an increased intrapancreatic acetylcholine activity. In an attempt to clarify these observations, the dose-inhibition effect of atropine, the dose-response effect of a cholinergic agonist and the effect of vagal stimulation on pancreatic protein output in alcoholic and normal dogs was compared. The inhibitory effect of atropine and the effect of vagal stimulation were unchanged but the sensitivity to exogenous cholinergic stimulation was decreased in alcoholic dogs compared to normals. It is suggested, that the chronic repetitive ethanol exposure of acinar muscarinic receptors, desensitizes them to cholinergic stimulation but induces paradoxical sensitivity to ethanol, while the interaction of atropine is left unchanged. The increased availability of acetylcholine would only be an adaptive phenomenon to the desensitization.

Animals↗
PubMed1988

A comparative study of the effects of four motor-stimulating agents on canine jejunal spike bursts. The use of a computer program to analyze spike burst spread.

The intestinal myoelectric effects of four motor-stimulating drugs were compared in conscious dogs. Dogs were fed a standardized 400-kcal meal, and the myoelectric activity was monitored before and after drug administration. Graded doses of metoclopramide, cisapride, bethanechol, and cholecystokinin (CCK) were compared by means of a computer program to identify spike bursts and determine their frequency, duration, and length of migration. Bethanechol and CCK produced the greatest increase in myoelectric activity in terms of spike burst frequency and duration but the least in terms of length of spike burst spread. Metoclopramide had minimal measurable myoelectric effects. Cisapride had the greatest effect on the length of spike burst migration but little effect on spike burst frequency and duration. The results suggest that cisapride is a more efficient prokinetic agent than bethanechol, CCK, or metoclopramide. The greater length of spike burst spread caused by cisapride was associated with a more rapid rate of transit along the monitored segment of bowel when compared with control. This confirms the correlation between length of spike burst spread and propulsive efficiency.

Animals↗
PubMed1992

Effect of ethanol intake on pancreatic exocrine secretion in mice.

Swiss mice were fed conventional lab chow and 10% ethanol or water as drinking fluid for 2 weeks. Pancreatic juice was obtained by cannulation of the bile pancreatic common duct of mice anesthetized with urethane. Isolated pancreatic lobules were also obtained. The flow rate and the amylase output were determined in pure pancreatic juice. The release of amylase was measured in pancreatic lobule preparations. The basal pancreatic juice flow rate and the amylase output were significantly increased by ethanol consumption. The magnitude of the pancreatic juice flow rate and the amylase output responses to increasing doses of bethanechol, a cholinergic agent, was significantly decreased in ethanol-fed mice. The amount of spontaneously released amylase was higher in pancreatic lobule preparations from ethanol-fed animals than that from control mice, and the difference was abolished by addition of atropine to the incubation media. The amylase release rate in response to increasing doses of bethanechol was significantly reduced in lobule preparations from the ethanol-fed group. These data indicate that ethanol intake in mice has a stimulating effect on the spontaneous pancreatic secretion and lends support to the hypothesis that ethanol consumption increases the intrapancreatic cholinergic tone.

Amylases↗
PubMed1978

The effects of norephedrine and bethanechol on the human urethral closure pressure profile.

In twelve women with urinary stress incontinence simultaneous measurements were made of the intravesical and intra-urethral pressures, including the urethral closure pressure profile (UCPP), before and after oral administration of norephedrine or subcutaneous injection of bethanechol. The investigations were carried out at various bladder volumes in the supine position and at bladder volume 300 ml in erect position. Irrespective of bladder volume or body position, norephedrine caused a statistically significant rise in maximum urethral pressure (MUP) and in maximum urethral closure pressure (MUCP). The intravesical pressure was not affected. After intravenous injection of phentolamine, MUP and MUCP fell to levels below the original readings, but here too the intravesical pressure was unaffected. Injection of bethanechol was followed by significant increase in the intravesical pressure, irrespective of bladder volume or body position. There were no consistent changes in the intra-urethral pressure. As a consequence of the rise in intravesical pressure, however, the MUCP fell slightly. The results of the study suggest that orally administered norephedrine causes an increase in the MUCP in women with stress incontinence of urine, an increase that may prove therapeutically useful. Bethanechol, in doses that significantly increased intravesical pressure, did not alter the intra-urethral pressure.

Administration, Oral↗
PubMed1989

Intracerebral drug delivery in rats with lesion-induced memory deficits.

Pharmacological treatments directed at increasing cortical acetylcholine activity in patients with Alzheimer's disease have largely been disappointing, perhaps because denervated areas of brain may not be exposed to adequate amounts of drug. A new method has been developed to enable localized intracerebral delivery of neurotransmitter substances using a polymeric drug delivery system. Microspheres of a polyanhydride sebacic acid copolymer were impregnated with bethanechol, an acetylcholinesterase-resistant cholinomimetic. Twenty rats received bilateral fimbria-fornix lesions, producing cholinergic denervation of the hippocampus and marked impairment in spatial memory. The animals were trained for 2 weeks to run after which they received bilateral intrahippocampal implants of saline (five rats), blank polymer (five rats), or bethanechol-impregnated polymer (10 rats). Following implantation, spatial memory was assessed by radial-maze performance testing for 40 days. Untreated lesioned rats showed persistently poor spatial memory, entering maze arms with near random frequency. Similarly, animals treated with saline and blank polymer did not improve after implantation. Rats treated with bethanechol-impregnated microspheres, however displayed significant improvement within 10 days after implantation; this improvement persisted for the duration of the experiment (p less than 0.05, Student's t-test). Histological analysis of regional acetylcholinesterase staining showed widespread loss of activity throughout the hippocampus bilaterally in all animals. The microsphere implants were visible within the hippocampus, with minimal reactive changes in surrounding brain. It is concluded that intracerebral polymeric drug delivery successfully reversed lesion-induced memory deficits, and has potential as a neurosurgical treatment method for Alzheimer's disease and other neurodegenerative disorders.

Anhydrides↗
PubMed1989

Intracerebroventricular bethanechol chloride infusion in Alzheimer's disease. Results of a collaborative double-blind study.

The use of intracerebroventricular bethanechol chloride infusion in patients with Alzheimer's disease was first reported in 1984. An initial trial in four patients demonstrated the feasibility of this approach for cholinergic drug delivery to the brain, but objective improvement in cognitive function was not documented. A collaborative placebo-controlled double-blind crossover study has now been carried out in 49 patients with biopsy-documented Alzheimer's disease. The results demonstrate a statistical improvement in Mini-Mental State scores and significantly slower performance on Trails A testing during drug infusion. Other neuropsychological test scores were not similarly affected. The degree of improvement was not sufficient to justify further treatment of Alzheimer's disease patients by intracerebroventricular infusion of bethanechol chloride. The drug delivery system used in the study was well tolerated, with two irreversible complications in more than 50,000 patient days.

Alzheimer Disease↗