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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↗
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↗
PubMed1983

Effects of metoclopramide and bethanechol on delayed gastric emptying present in gastroesophageal reflux patients.

Gastric emptying has been reported to be delayed in a significant percentage of patients with gastroesophageal reflux. The rationale for the use of metoclopramide and bethanechol in gastroesophageal reflux has been based on their ability to stimulate lower esophageal sphincter pressure and enhance acid clearance mechanisms. In this study, we investigated the comparative efficacies of metoclopramide and bethanchol in improving the rate of gastric emptying in gastroesophageal reflux patients in whom delayed emptying was present. Gastric emptying studies used an isotope-labeled mixed solid-liquid meal. Thirteen reflux patients with delayed gastric emptying received metoclopramide, 10 mg intramuscularly, and subcutaneous bethanechol, 0.07 mg/kg, in a randomized single-blind fashion. Eleven additional reflux patients with delayed gastric emptying received oral metoclopramide, 10 mg, in an open-labeled fashion. After parenteral metoclopramide, gastric emptying was significantly (p less than 0.05) faster compared with both the initial basal day and the bethanechol treatment day. Compared with the normal gastric emptying rate established in 26 control subjects, metoclopramide accelerated gastric emptying into the normal range. Bethanechol did not increase gastric emptying. Metoclopramide orally also significantly improved gastric emptying. Our study indicates that metoclopramide, both parenterally and orally, increased the rate of gastric emptying in those reflux esophagitis patients in whom it was delayed, while bethanechol did not improve the degree of gastric retention in the same patients. Our results extend the rationale for the therapeutic efficacy of metoclopramide in gastroesophageal reflux disease.

Bethanechol↗
PubMed1977

Effect of bethanechol on gastroesophageal reflux.

In this study we determined the acute effect of bethanechol (5 mg SC) on gastroesophageal reflux (GER) and lower esophageal sphincter pressure (LESP) in 27 patients with symptomatic esophagitis. The effect of bethanechol on esophageal acid clearance was also determined in 7 of the patients. Intraluminal pH monitoring prior to bethanechol administration demonstrated free or stress-induced reflux episodes in 18 of the 27 patients. Following bethanechol (1) LESP increased significantly, (2) GER diminished or ceased in many of the patients, and (3) acid clearance times decreased significantly. Some individuals, however, continued to reflux despite LESP elevation to 30 mm Hg or more. This latter finding suggests that LESP alone is not the sole factor governing LES competency. Other factors such as improved esophageal emptying may also contribute to the beneficial therapeutic effect of bethanechol in patients with heartburn.

Bethanechol Compounds↗
PubMed1981

Effect of bethanechol on gastric functions in primary anorexia nervosa.

We have shown previously that patients with primary anorexia nervosa (PAN) have decreased gastric emptying and acid output. The present studies were designed to explore the possibility that bethanechol, a parasympathomimetic agent, would acutely restore normal gastric function in those patients. We used a dye dilution technique to determine acid output and fractional emptying rate in 5 patients with PAN and 11 healthy controls during a basal period and following bethanechol (0.06 mg/kg, subcutaneously). Although bethanechol caused fractional emptying and acid output to increase threefold in PAN (P less than 0.05), it failed to produce stimulation of gastric emptying and acid output to levels similar to those achieved in controls. Therefore, gastric emptying and acid output were less in PAN than in controls, both basally and after bethanechol. Since bethanechol failed to completely restore acute gastric function, the defect of emptying and acid output in PAN does not appear to be caused by a deficiency of parasympathetic neurotransmitter but, instead, could reflect undetermined inhibitory influences or impaired function of the muscular and glandular cells. Following weight gain, fractional emptying rate and acid output were still slightly less in PAN patients than in controls, but the difference was statistically significant only for basal acid output.

Adolescent↗
PubMed1987

Binding of the S(+)- and R(-)-enantiomers of bethanechol to muscarinic receptors in jejunal smooth muscle, nasal mucosa, atrial and ventricular myocardium of the rat.

Both the enantiomers of bethanechol displaced R(-)-[3H]quinuclidinyl benzilate from muscarinic binding sites in homogenates from rat jejunum, nasal mucosa, atrial and ventricular myocardium. Stereoselectivity of receptor binding for S(+)- and R(-)-bethanechol was found in all tissues investigated (Ki S(+) less than Ki R(-)). Different proportions of high and low affinity binding sites for bethanechol enantiomers and S(+)-methacholine in jejunal smooth muscle, atrial and ventricular muscle and the presence of only low affinity binding sites in nasal mucosa point to differences in receptor-effector coupling in these tissues. The relative insensitivity of cardiac tissue for bethanechol compared to methacholine might be related to the much smaller proportion of high affinity binding sites found for S(+)-bethanechol in heart ventricular muscle.

Animals↗
PubMed2003

Study of the afferent nervous system and its evaluation in women with impaired detrusor contractility treated with bethanechol.

OBJECTIVES: To study the effects of subcutaneous bethanechol on the afferent nervous system and correlate these with the efficiency of this treatment in women with impaired detrusor contractility and to evaluate whether patients likely to respond to bethanechol can be identified before treatment through sensation evaluation. METHODS: Eighteen women with impaired detrusor contractility were given subcutaneous bethanechol for 10 days, and the flow pattern and postvoid residual urine volume were monitored. The afferent nervous system was studied before and after therapy by evaluating the sensation of filling during cystometry and by determining the bladder electrical perception threshold (EPT). RESULTS: At the end of therapy, 61% voided without a postvoid residual volume. In these women, the sensation of filling and electrical sensitivity were significantly increased compared with before treatment. In women who still voided with a postvoid residual volume, the sensation of filling had increased to a lesser extent and no change in EPT was found. Women in whom bethanechol was unsuccessful had a higher pretreatment EPT than women who were successful. No such difference was found for the sensation of filling. CONCLUSIONS: An increase in bladder sensitivity correlated with improvement in bladder emptying and can be evaluated by studying the sensation of filling and EPT. Patients likely to respond to bethanechol can be identified before treatment on the basis of the EPT level. Therefore, it would be valuable to initiate EPT measurement in the diagnosis of patients with impaired detrusor contractility.

Adult↗
PubMed1982

Trophic effects of chronic bethanechol on pancreas, stomach, and duodenum in rats.

Rats received a daily injection of 2, 6, or 12 mg kg-1 bethanechol for 7 or 14 days. Pancreatic weight and content of protein, amylase, and chymotrypsinogen were increased in a dose and time dependent fashion by bethanechol. After 14 days of treatment with the highest dose, pancreatic weight and total pancreatic DNA content increased to 1.18 times control (P less than 0.05) while protein increased to 1.25, amylase to 1.85, and chymotrypsinogen to 1.72 times control. There was a slight increase in oxyntic gland area weight in bethanechol-treated rats, but content of DNA, protein, and pepsinogen were not changed. Bethanechol had no effect on duodenal weight or content of DNA, protein, or maltase. Acute administration of 12 mg kg-1 bethanechol increased circulating gastrin levels for at least 4 h in unanesthetized rats. We conclude that long-term treatment with a cholinergic agonist produces pancreatic hyperplasia and increases protein and enzyme content. Under the conditions of this study, no effects were seen on oxyntic gland area of stomach or duodenum.

Animals↗
PubMed1979

Effect of bethanechol, gastrin I, or cholecystokinin on myoelectrical activity.

The purpose of this study was to determine the effect of bethanechol, gastrin I, or the octapeptide of cholecystokinin (CCK-OP) on the smooth muscle of the isolated cat colon. Myoelectrical activity was recorded with monopolar glass-pore electrodes. Slow-wave frequency was 5.9 +/- 0.2 cycles/min during the basal period. Slow waves were generally coupled during the control period and the apparent propagation velocity was predominantly aborad at a velocity of 3.8 +/- 0.4 mm/s. Spike activity was superimposed on 11.9 +/- 1.5% of the slow waves during the control period. Bethanechol stimulated a dose-dependent increase in colonic spike activity, with a threshold concentration of 10(-7) M. Bethanechol did not alter the congruence of the colonic slow-wave frequency at any concentration. Gastrin I or CCK-OP increased colonic spike activity. The threshold concentrations for gastrin I and CCK-OP were 2 X 10(-11) M and 4 x 10(-11) M, respectively. Unlike bethanechol, gastrin I (2 X 10(-9) M - 2 X 10(-8) M) and CCK-OP (4 X 10(-9) - 4 X 10(-8) M) altered slow-wave frequency and decreased slow-wave congruence. These studies suggest that 1) bethanechol, gastrin I, or CCK-OP increases colonic spike activity, and 2) only gastrin I or CCK-OP alters the slow-wave frequency of colonic muscle. Thus neurohumoral substances may act independently on colonic spike activity and colonic slow-wave frequency.

Action Potentials↗
PubMed1997

Bethanechol chloride oral solutions: stability and use in infants.

OBJECTIVE: To assess the stability of a bethanechol chloride oral solution prepared from tablets. METHOD: The initial concentrations were determined. These solutions were stored at 4 degrees C for 90 days. During this period, the concentrations of the bethanechol chloride solutions were determined by spectrophotometry. The clinical efficacy of the oral solution was tested in five infants with gastroesophageal reflux disease by comparison of gastric pH before and after treatment. RESULTS: Significant decomposition of bethanechol chloride occurred in the two formulations. Bethanechol oral solution in sterile water for irrigation was well tolerated by five pediatric patients, and the clinical efficacy was equivalent to that of the tablet formulation. CONCLUSIONS: The bethanechol chloride oral solution 1 mg/mL in sterile water for irrigation was stable at least 30 days when stored at 4 degrees C and at an initial pH of 6.5. This formulation appears to be clinically acceptable and provides a convenient dosage form for use in pediatric patients.

Bethanechol↗
PubMed1980

Reflux esophagitis: effect of oral bethanechol on symptoms and endoscopic findings.

We ascertained the effectiveness of oral bethanechol on symptoms and endoscopic evaluation of reflux esophagitis in a double-blind controlled study. Forty-four patients were treated with either 25-mg bethanechol tablets or placebo, each given four times daily for 4 weeks, in addition to conventional medical therapy. Both therapies significantly decreased symptoms as well as endoscopic lesions; however, endoscopic improvement was significantly better in the bethanechol-treated group. Bethanechol therapy resulted in complete endoscopic healing in 10 of 22 cases, whereas only three of 22 patients in the control group had such healing. No worsening of endoscopic lesions was seen in either group. Our study indicates that bethanechol is an effective drug offering advantages over conventional antacid therapy in the treatment of reflux esophagitis.

Administration, Oral↗
PubMed1982

Double-blind controlled trial of bethanechol and antacid versus placebo and antacid in the treatment of erosive esophagitis.

To determine the value of bethanechol in the treatment of erosive esophagitis, a double-blind study was undertaken in which 28 patients were randomized to either bethanechol and antacid, or placebo and antacid. Patients were evaluated clinically, endoscopically, and by esophageal manometry before and after 8 wk of therapy. After treatment both groups showed significant improvement in heartburn and in healing of esophageal lesions. Patients who received bethanechol plus antacids did not show a greater improvement than patients who received placebo plus antacids in any category, nor did patients in the bethanechol-treated group have a greater incidence of complete healing. In addition, pretreatment mean lower esophageal sphincter pressure was normal in approximately 30% of patients with erosive esophagitis and this finding was associated with a greater chance for complete healing of esophageal lesions. These results fail to show that the addition of bethanechol to an intensive antacid regimen is more effective than the antacid regimen alone in the treatment of erosive esophagitis and that patients with esophagitis and normal lower esophageal sphincter pressures respond more favorably to medical treatment.

Antacids↗
PubMed1992

Bethanechol and a G-protein activator, NaF/AlCl3, induce secretory response in Paneth cells of mouse intestine.

Paneth cells located at the bottom of intestinal crypts may play a role in controlling the bacterial milieu of the intestine. Using morphometry to clarify the secretory mechanism of the Paneth cells, we studied the ultrastructural changes in mouse Paneth cells produced following intra-arterial perfusion with Hanks' balanced salt solution containing a cholinergic muscarinic secretagogue (bethanechol), a neuroblocking agent (tetrodotoxin), or a G-protein activator (NAF/AlCl3). Bethanechol (2 x 10(-4) mol/l) induced Paneth-cell secretion. Many Paneth cells massively exocytosed their secretory material into the crypt lumen; the enhanced secretion caused degranulation and vacuole formation. However, tetrodotoxin (2 x 10(-6) mol/l) did not prevent the bethanechol-enhanced secretion by the Paneth cells. NaF (1 x 10(-2) mol/l) and AlCl3 (1 x 10(-5) mol/l) induced massive exocytosis of the Paneth cells; the exocytotic figures were similar to those observed in mice stimulated by bethanechol. G-protein activation was followed by a sequence of intracellular events, resulting in exocytosis.

Aluminum↗
PubMed1988

Bethanechol-induced increase in hypothalamic estrogen receptor binding in female rats is related to capacity for estrogen-dependent reproductive behavior.

Neuroactive agents associated with different neurotransmitter systems can modulate the number of hypothalamic estrogen binding sites. It has been demonstrated previously that the muscarinic cholinergic agonist, bethanechol, administered 30 min prior to in vitro estrogen receptor assays increases the concentration of hypothalamic estrogen binding sites by 30-35% in female rats. Bethanechol was without effect on male hypothalamic preparations. In order to investigate further this sex difference and in an attempt to determine a relationship between the modulation of estrogen binding sites and a sexually differentiated function, bethanechol was given to female rats rendered either anovulatory and capable of displaying lordosis or anovulatory and behaviorally insensitive to estrogen. The results showed that bethanechol significantly increased the number of estrogen binding sites in females capable of displaying lordosis but not in females which did not show this estrogen-dependent behavior. It is possible that the capacity for drug-induced modulation of estrogen binding sites could be related functionally to the ability to display lordosis behavior.

Animals↗
PubMed1989

Detection of missing vesicoureteral reflux with bethanechol chloride-aided voiding cystourethrography.

Experience in the detection of absent vesicoureteral reflux with bethanechol-aided voiding cystourethrography is presented. The detection rate with conventional contrast-enhanced voiding cystourethrography among 9 study subjects, in whom vesicoureteral reflux otherwise was highly suspected from accompanying clinical, urographic and endoscopic features, and in whom it was absent contralaterally or bilaterally, was improved from 33 per cent (only 3 of 9 patients were positive for reflux) to 100 per cent (all 9 were proved to have vesicoureteral reflux) after bethanechol stimulation. Some representative cases are presented and the mechanisms of inducing vesicoureteral reflux with bethanechol are discussed as well as its clinical relevance. Bethanechol-aided voiding cystourethrography is suggested as a highly sensitive method to detect absent vesicoureteral reflux.

Adult↗
PubMed1982

Bethanechol chloride and the traumatic cord bladder.

The effect of bethanechol chloride was evaluated in 28 men with neurogenic bladder disease secondary to traumatic spinal cord damage. Simultaneous measurements of bladder pressure, electromyography of the pelvic floor and flow rate were obtained to evaluate the effect on voiding. The results of these studies revealed that bethanechol chloride failed to improve voiding dysfunction in these patients in either the supine or sitting position. Functional bladder outlet obstruction was aggravated by bethanechol chloride. It was found that the effect of this drug on the bladder was unpredictable, as evidenced by some patients converting from a definite detrusor contraction to a wave type pattern. Bethanechol chloride failed to induce a detrusor contraction in patients with areflexia or wave pattern bladders.

Adult↗
PubMed1982

Effect of bethanechol on gastric acid secretion and serum gastrin concentration after proximal gastric vagotomy.

It has been suggested that maximal acid output decreases after vagotomy as a result of reduced cholinergic activity and that maximal acid secretion can be restored to prevagotomy levels with cholinergic agonists. To test this, a maximally tolerated dose of bethanechol (50 micrograms/kg/hr) or saline was infused intravenously in nine duodenal ulcer patients who had been treated by proximal gastric vagotomy. Bethanechol infusion significantly (p less than 0.05) increased basal acid secretion without affecting basal serum gastrin concentrations. Despite stimulation of basal acid secretion, bethanechol had no significant effect on maximal acid output in response to subcutaneous pentagastrin. Although bethanechol significantly increased maximal acid output in response to subcutaneous histamine, maximal acid secretion in response to histamine (or to pentagastrin) was not restored to the prevagotomy level in any patient. Thus, factors other than loss of cholinergic activity appear to be responsible for the large reduction in maximal secretory capacity after vagotomy.

Adult↗
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↗