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PubMed1986

The effect of acid and bethanechol stimulation in patients with symptomatic hypertensive peristaltic (nutcracker) esophagus. Evidence that this disorder may be a precursor of diffuse esophageal spasm.

The hypertensive peristaltic (nutcracker) esophagus represents a motility disorder characterized clinically by squeezing retrosternal chest pain and manometrically by high amplitude esophageal peristaltic contractions. This study was designed to examine whether the nutcracker esophagus is: (a) a distinct entity, (b) a member of the spectrum of primary esophageal dysmotilities (e.g., diffuse esophageal spasm and achalasia), or (c) is secondary to reflux-induced acid sensitivity. Thirteen patients with a nutcracker esophagus by baseline manometry were subsequently studied after acid perfusion and bethanechol stimulation (0.08 mg/kg). Records were analyzed for symptomatic response and motility changes. Eight of 13 (62%) experienced chest pain during acid perfusion, but none had significant motility changes documented during this period. After bethanechol injection, chest pain occurred in six of 12 (50%) patients; two had burning pain and in the other four (33%) their squeezing chest pain was reproduced. Changes in the motility tracing with evidence of disordered motility suggestive of diffuse esophageal spasm were seen after bethanechol in seven of the 12 tracings analyzed (58%), including all six patients who developed chest pain. We conclude that patients with nutcracker esophagus on baseline manometry may develop motility patterns consistent with diffuse esophageal spasm after provocation with bethanechol. We take this to suggest that the nutcracker esophagus is part of the continuum of primary motility disorders and may actually be a precursor of diffuse esophageal spasm.

Adult↗
PubMed1986

A critical review of current medical therapy for gastroesophageal reflux disease.

Gastroesophageal reflux (GER) disease is a common, multifactorial medical condition that may be difficult to treat. Simple lifestyle modifications decrease reflux episodes and should serve as the cornerstone for medical therapy. Antacids or alginic acid may be helpful in mild disease but recent studies suggest they may be no better than placebo. Metoclopramide improves symptomatic GER disease but side effects are a major limiting factor. Only bethanechol and the histamine H2 antagonists have been conclusively shown to improve esophagitis significantly. Therefore, more severe disease is currently best treated with a histamine H2 antagonist alone or in combination with bethanechol. The treatment of GER complications and maintenance therapy have only been recently addressed in clinical trials, but again the histamine H2 antagonists may have a useful role. Five to 10% of patients may require antireflux surgery, but the competency of the repair appears to deteriorate with time. Future clinical trials need to address specific areas of difficulty including entry criteria, test of efficacy, study duration, and usefulness of combination drug therapy.

Alginates↗
PubMed1987

Effects of long-term medical treatment with cimetidine and bethanechol in patients with esophagitis and Barrett's esophagus.

To evaluate long-term medical therapy in patients with Barrett's esophagus, six patients were studied before and after long-term therapy with cimetidine for a mean period of 11.7 months. Some patients also received bethanechol. All had severe symptoms of gastroesophageal reflux resistant to intensive antacid therapy, specialized columnar epithelium by biopsy, and endoscopic evidence of severe inflammation. Esophageal manometry documented a hypotensive lower esophageal sphincter in three patients and low peristaltic amplitude in the distal esophagus in four. Treatment was begun with cimetidine, 300 mg orally four times daily. If symptoms did not totally abate, bethanechol, 25 mg orally four times daily, was added. Cimetidine completely relieved or dramatically reduced symptoms in all patients. Adding bethanechol produced further symptomatic improvement in three of four patients. After initial dilatation in the two patients with strictures, there was no recurrence. Endoscopic evidence of inflammation resolved completely in four patients and was markedly improved in two. Treatment with both drugs was well tolerated by all patients. The abnormally placed squamo-columnar junction did not regress during follow-up.

Adult↗
PubMed1990

Bicarbonate secretion in isolated guinea pig antrum.

HCO3- secretion was investigated in isolated guinea pig antral mucosa mounted in Ussing chambers. The rate of HCO3- secretion was measured by a pH-stat system. The antral mucosa spontaneously secreted HCO3- at a rate of about 0.5 microEq cm-2 h-1. Bethanechol (100 microM) or 8-bromoadenosine 3':5'-cyclic monophosphate (8-Br-cAMP, 1 mM) induced a significant increase in HCO3- secretion. Prostaglandin E2 (1 microM) also produced an increase in HCO3- secretion, although it was less effective than either bethanechol or 8-Br-cAMP. Histamine (100 microM) did not affect HCO3- secretion. This preparation may be suited to the study of the precise mechanisms by which neurohumoral factors regulate gastric HCO3- secretion.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1986

Early effects of bethanechol on the esophageal motor function of infants with gastroesophageal reflux.

Lower esophageal sphincter (LES) pressure, as well as esophageal peristaltic amplitude, duration, and velocity were measured in 16 infants with gastroesophageal reflux before administration of subcutaneous bethanechol, and at 10, 20, and 30 min after. Seven infants received 0.1 mg/kg, and 9 received 0.2 mg/kg. Significant increases in LES pressure occurred at both doses and lasted for 20 min. The amplitude and duration of peristaltic contractions were increased only after the larger bethanechol dose, and the increases were of greater magnitude in the distal esophagus than in the middle esophagus. The velocity of peristalsis decreased significantly in both the lower and middle esophagus, but only after the larger dose of bethanechol. Bethanechol had no effect on any motor function of the upper third of the esophagus. The changes in esophageal peristalsis produced by bethanechol may improve the efficiency of distal esophageal acid clearance and thus may be responsible in part for the therapeutic effect of bethanechol in infants with gastroesophageal reflux.

Bethanechol↗
PubMed1986

Effect of bethanechol and metoclopramide on upper gastrointestinal motility in the kitten.

Gastroesophageal reflux (GER) during infancy is a disorder of unknown etiology which may be associated with abnormalities of upper gastrointestinal motor function. Bethanechol, a muscarinic agonist, and metoclopramide, a dopamine antagonist, have been utilized as pharmacologic agents in an attempt to improve upper gastrointestinal motility in this disorder. We have studied the effect of these agents on upper gastrointestinal motility in an infant model, the kitten. Bethanechol is found to greatly increase lower esophageal sphincter (LES) pressure and have no effect on esophageal peristaltic amplitude or gastric emptying of a liquid meal. Metoclopramide causes a small and nonsignificant increase in LES pressure, has no effect on esophageal peristalsis, and increases the rate of gastric emptying of a liquid meal. These results suggest that these two agents may have specific actions on the infant's upper gastrointestinal tract.

Animals↗
PubMedDate not supplied

Bethanechol for pediatric gastroesophageal reflux: a prospective, blind, controlled study.

To investigate the effect of bethanechol on postprandial gastroesophageal reflux in children, and the relationship between its effect on the lower esophageal sphincter pressure and its effect on reflux, we studied 31 consecutive children with pathologic reflux, using manometry and pH probe, both before and after administration of bethanechol. The initial sphincter pressure was subnormal in only 35% of the patients. The bethanechol-treated sphincter pressure was increased in 97% of the patients (from 13.4 +/- 1.3 to 34.1 +/- 2.6 mm Hg) and was normal in 97% of the patients, yet bethanechol did not improve any measure of postprandial reflux in the patient group as a whole. Furthermore, the 20 patients with normal sphincter pressures had significant worsening of their percent of postprandial time with reflux (from 21.8 +/- 5.3 to 33.8 +/- 6.0%, p = 0.009). Thus, this study demonstrates a failure of the acute administration of bethanechol to improve postprandial gastroesophageal reflux and raises the issue of whether the widespread use of bethanechol to treat reflux in children is appropriate.

Bethanechol Compounds↗
PubMed1990

Muscarinic control of gallbladder dynamics. A study using 99Tcm-HIDA and cholinergic agonists and antagonists.

We studied 12 normal subjects who underwent four 99Tcm-HIDA examinations. Imaging was performed with 111 MBq at 1 image/min for 60 min, and was registered on a computer on a 64 x 64 word matrix. Normalized and background corrected time-activity curves on the gallbladder were obtained from which total and cumulative 10 min interval emptying was calculated. During the first examination (control), 10 min after the beginning of acquisition, 1 ml saline solution was injected subcutaneously. The second examination was performed injecting 5 mg bethanechol subcutaneously instead of saline solution. During the third and fourth examinations 10 mg pirenzepine and 0.15 mg/10 kg atropine were injected i.v. respectively, 5 min before bethanechol injection. Wilcoxon's test was used to compare the first and second studies and the latter with the third and fourth studies. The median value of gallbladder emptying at 60 min was 2% with saline solution injection and 27.5% with bethanechol. This difference was significant from minute 30 onwards. Atropine administration inhibited gallbladder emptying completely in all cases, with significant differences (P less than 0.01) in relation to bethanechol values following the first 30 min of the examination. Gallbladder emptying was observed in the study with pirenzepine, but was significantly inferior to the bethanechol values after the first 30 min.

Adult↗
PubMed1986

Stimulatory effect of hypercalcemia on pancreatic secretion is prevented by pretreatment with cholecystokinin and cholinergic agonists.

Recently, we demonstrated that hypercalcemia causes marked stimulation of feline exocrine pancreatic secretion, and that this effect is absent when a large dose of cholecystokinin (CCK) is infused prior to induction of hypercalcemia. To investigate this effect in more detail, anesthetized cats were given calcium i.v. after preadministration of CCK or urecholine (a cholinergic agonist) at specific doses, or of saline as a control. We found that the hypercalcemia-induced stimulation of pancreatic protein secretion was abolished after preadministration of CCK at large doses. After the prestimulus dose was decreased or the calcium dose was increased, however, the pancreatic secretory response to hypercalcemia was preserved. In contrast, the response to a submaximal dose of CCK was unchanged after prestimulation with a large dose of CCK. Similar results were obtained when urecholine instead of CCK was used as prestimulus. These findings indicate that loss of pancreatic responsiveness to hypercalcemia following prestimulation with CCK is dependent on doses of both prestimulus and calcium used, and that it is not specific for prestimulation with CCK but also inducible by cholinergic agonists. They further suggest that this phenomenon is not due to exhaustion of pancreatic secretory capacity, but may reflect decreased sensitivity to the hypercalcemic stimulus instead.

Animals↗
PubMed1986

Effects of bethanechol on the pancreas in antrectomized and normal rats.

The effect of chronic administration of bethanechol and pentagastrin on the pancreas was examined. Rats were either antrectomized or subjected to a sham operation. Three weeks after surgery, rats received a daily intraperitoneal injection of either bethanechol (12 mg/kg) or pentagastrin (250 micrograms/kg) for 14 days. The fasting serum gastrin after bethanechol treatment increased to 1.89 times that of controls treated with saline. Although antrectomy decreased fasting serum gastrin to approximately 40% of controls, serum gastrin increased by 2.17 times that of the antrectomized rats and 1.37 times that of controls in the bethanechol group. After 14 days of bethanechol treatment, weight and amylase in the pancreas increased significantly compared with control; DNA and protein also increased 1.3 and 1.5 times that of control. The increase in DNA and pancreatic weight indicated that hyperplasia was the predominant mechanism. The pancreas showed atrophy in antrectomized rats but this was reversed by both bethanechol and pentagastrin. The results indicate that either endogenous gastric or extragastric gastrin release by cholinergic stimuli may have an important role in the regulation of pancreatic growth.

Animals↗
PubMed1988

Effect of peptide YY on insulin release stimulated by 2-deoxyglucose and neuropeptides in dogs.

Peptide YY (PYY) is a hormone released from gut after a meal. The objective of this study was to determine the effect of PYY on insulin release stimulated by either 2-deoxyglucose (2-DG) or neuropeptides in conscious dogs with gastric and duodenal fistulas. In control experiments dogs received either 2-DG (75 mg/kg i.v. bolus) or atropine (25 micrograms/kg bolus followed by 20 micrograms/kg/h i.v.) plus 2-DG (75 mg/kg i.v.) or bethanechol (80 micrograms/kg/h i.v.) or vasoactive intestinal peptide (VIP, 4 micrograms/kg i.v. bolus) or gastrin-releasing peptide (GRP, 400 pmol/kg/h i.v.) or tetragastrin (G4, 100 micrograms/dog, i.v. bolus). On separate days, PYY was also infused intravenously in combination with one of the above stimulants. Given intravenously, PYY (200, 400 pmol/kg/h) significantly inhibited 2-DG stimulated-insulin secretion in a dose-dependent fashion. This inhibitory effect also existed in the presence of atropine. Peptide YY (400 pmol/kg/h) depressed the insulin levels in response to GRP or G4 but failed to inhibit bethanechol- and VIP-stimulated insulin release. After administration of the above stimulants, PYY did not modify the blood sugar concentrations. These results demonstrated that PYY might inhibit the cephalic phase of insulin release from dogs triggered by 2-DG and by the neuropeptides GRP and G4. Thus, PYY may play a negative feedback regulatory role on insulin release.

Animals↗
PubMed1989

Subtypes of muscarinic receptors in pancreatic exocrine secretion in anesthetized dog.

Characterization of muscarinic receptor subtypes on the dog pancreas in situ was examined by using specific muscarinic receptor antagonists to study pancreatic exocrine secretion. Bethanechol caused an increase in pancreatic exocrine secretion, with a high concentration of protein and little effect on bicarbonate concentration. Thus bethanechol may mainly affect the muscarinic receptors of the acinar cells. Bethanechol-stimulated secretion was inhibited by pirenzepine (a specific M1 muscarinic antagonist), 4-diphenylacetoxy-N-methylpiperidine methobromide (4-DAMP, a specific M3 muscarinic antagonist), and atropine (a mixed muscarinic receptor antagonist). However, [11-[[2-(diethylamino)methyl]-1-piperidinyl]acetyl]-5, 11- dihydro-6H-pyrido[2,3-b][1,4]benzo-diazepine-6-one (AF-DX 116, a specific cardioselective M2 antagonist) did not have any effects on bethanechol-stimulated secretion. Increased protein secretion in pancreatic juice stimulated by bethanechol was significantly inhibited by 4-DAMP and atropine and was suppressed by pirenzepine, but was not modified by AF-DX 116. Bicarbonate concentration was not modified by these antagonists. 4-DAMP, atropine, and pirenzepine caused a progressive parallel rightward shift in the dose-response curve of pancreatic secretion for bethanechol. Schild analysis of the data indicated a pA2 value of 8.7 for 4-DAMP, 7.9 for atropine, and 6.2 for pirenzepine, respectively. Thus 4-DAMP has 7.5 times and 440 times greater potency than atropine and pirenzepine to inhibit bethanechol-stimulated secretion. The slope of the Schild regression line was not different from 1. These results suggest that inhibitions of bethanechol-stimulated pancreatic secretion are competitive for 4-DAMP, atropine, and pirenzepine and that bethanechol-stimulated pancreatic secretion is mediated by M3 muscarinic receptors in dogs.

Animals↗
PubMed1989

Exocrine pancreas in rabbits fed a copper-deficient diet: structural and functional studies.

The effects of a copper-deficient diet supplemented with D-penicillamine on both the structure and exocrine function of the pancreas were studied in rabbits. The pancreases of the animals kept on this diet for 13 weeks showed lesions in the acinar tissue but not in ductal or islet tissue. The weights of the glands were markedly reduced. Copper deficiency caused a slight (non-significant) reduction in the flow of pancreatic juice and in sodium output and significantly decreased chloride output (p less than 0.01). No changes were observed in bicarbonate and potassium output. Total protein and amylase secretions were maintained at clearly detectable levels in pancreatic juice, although they decreased significantly (p less than 0.01 and p less than 0.001, respectively), in the copper-deficient animals compared with the controls. The pancreases of the animals kept on a copper-deficient diet were seen to maintain their capacity for response to secretin, cholecystokinin (CCK), and bethanechol. Our results show that rabbit pancreatic acinar tissue is less sensitive to copper deficiency than that of other species studied. Additionally, the data on secretion of water and electrolytes suggest that in the rabbit the acinar cells may contribute to the secretory process with a chloride-rich fluid.

Amylases↗
PubMed1990

Differing effects of ethanol on in vitro stimulated pancreatic enzyme secretion in ethanol-fed and control rats.

The single most important risk factor for chronic and acute pancreatitis is the abuse of ethanol, which, theoretically, could affect the pancreas by interacting either with some of its cell receptors or with any of its intracellular signal transduction mechanisms. Therefore, we determined in isolated pancreatic acini from 3 month ethanol-fed rats and controls the dose-response effects of secretagogues on enzyme secretion, both in the presence and absence of ethanol in the incubation medium. In ethanol-fed rats, pancreatic amylase activity was decreased by 40%, compared to controls (with identical carbohydrates intakes), whereas lipase and trypsinogen activities were unaffected. With no ethanol in the incubation medium, basal enzyme releases and enzyme dose-response curves to CCK-8, VIP, secretin, bombesin, and bethanechol were essentially unchanged in ethanol-fed rats compared to controls. In contrast, with 0.1 M ethanol present in the medium, enzyme responses to VIP, secretin, and CCK-8 were inhibited and that to CCK-8 also shifted to the right in ethanol-fed rats compared to controls. Hence, if rechallenged to ethanol, acini from ethanol-fed rats show inhibited secretions, in response to two secretagogues acting through the release of cyclic AMP, and an inhibited and right-shifted secretory response to CCK.

Amylases↗
PubMed1993

Cholinergic regulation of phase II interdigestive pancreatic secretion in humans.

Small fluctuations in cholinergic input may be involved in the regulation of human interdigestive pancreatic secretion. To determine the effects of small changes in cholinergic tone on phase II interdigestive trypsin secretion, we gave cholinergic agonists or antagonists to 17 healthy fasting subjects who underwent gastrointestinal intubation. Duodenal trypsin outputs, gastroduodenal motility, and plasma levels of pancreatic polypeptide (PP) as a marker of cholinergic tone were measured during intravenous infusion of bethanechol (0, 5, or 40 micrograms.kg-1.h-1) or atropine (0, 4, or 16 micrograms.kg-1.h-1) given during phase II alone or in combination based on a 3 x 3 factorial design. Data were evaluated by a response surface analysis of the average log values for the test period (using the average of log values of the control period as a covariate). Bethanechol increased trypsin output (p < 0.05) and plasma concentrations of PP (p < 0.05) within the ranges of spontaneous fluctuations of trypsin output and PP during phase II, but did not disrupt the periodicity of pancreatic secretion or the characteristic cyclical pattern of interdigestive motility and induction of phase III activity. Atropine markedly decreased trypsin output (p < 0.05) and plasma concentrations of PP (p < 0.05) and abolished the cycling of interdigestive pancreatic secretion and motor activity. These data suggest the hypothesis that cholinergic pathways participate in the control of interdigestive pancreatic secretion during phase II, while enzyme secretion during phase III may be regulated by other mechanisms.

Acetylcholine↗
PubMed1977

Diabetic visceral neuropathy: treatment with bethanechol chloride.

An 86-year-old diabetic man developed nausea, emesis, abdominal distention, and decreased gastrointestinal motility. A Hollander test confirmed incomplete vagal dysfunction. Treatment with bethanechol chloride resulted in marked improvement which was reproducible after withdrawal and reinstitution of therapy. We believe that treatment with bethanechol chloride deserves further investigation in selected patients with diabetic visceral neuropathy.

Aged↗