Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Bethanechol Compounds”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 145 records · Page 8Linked to original sources
PubMed1979

Effects of endogenous hyperglucagonemia on lower esophageal sphincter pressure and gastric acid secretion.

Lower esophageal sphincter function and gastric acid secretion were studied in a patient with endogenous hyperglucagonemia due to a functioning islet cell carcinoma. Complete resection of the tumor resulted in a fall of the serum concentration of immunoreactive glucagon to a normal level. Pre- and postoperative resting lower esophageal sphincter pressures and lower esophageal sphincter pressure responses to administration of pentagastrin, edrophonium, and bethanechol were unchanged. After surgery, preoperative immunoreactive glucagon concentrations were reproduced by intravenous infusion or intramuscular injection of exogenous glucagon. Lower esophageal sphincter resting pressures and responses to agonists were unchanged. In contrast, glucagon administered at 36 micrograms/kg/hr, which produced a serum concentration of immunoreactive glucagon (32,000 pg/ml) much greater than observed preoperatively (1200 pg/ml), diminished resting lower esophageal sphincter pressure and sphincter responses to pentagastrin, edrophonium, and bethanechol. Similarly, pentagastrin-stimulated gastric acid secretion was unaffected by tumor resection or low-dose glucagon infusion but was decreased at a glucagon infusion rate of 36 micrograms/kg/hr. This series of observations supports the thesis that endogenous glucagon plays no physiological role in the regulation of lower esophageal sphincter pressure or gastric acid secretion.

Adenoma, Islet Cell↗
PubMed1993

Altered esophageal pain threshold in irritable bowel syndrome.

Gut motility disorders and altered pain perception were reported in patients with irritable bowel syndrome (IBS). To verify foregut involvement in IBS, we studied 30 patients using esophageal manometry and 24-hr pH monitoring of the distal esophagus. Two subgroups of patients underwent esophageal provocative tests (bethanechol 50 micrograms/kg subcutaneously and esophageal balloon distension test). Twelve healthy volunteers formed a control group. A pain threshold on esophageal distension significantly lower than in healthy subjects (11.5 +/- 1 ml vs 22.2 +/- 1.7 ml, P < 0.01) was found in IBS patients. On the other hand, no differences between patients and controls were detected in lower esophageal sphincter pressure and length, esophageal body motility, or GER pattern; furthermore, bethanechol stimulation elicited similar esophageal body motility changes. Our study could confirm no detectable basal or bethanechol-induced esophageal motility disorders in IBS patients, nor enhanced GER. Esophageal involvement in IBS consists of a lower pain threshold on esophageal distension, possibly reflecting an altered visceral receptor sensitivity or modulation throughout the gut.

Adult↗
PubMed1986

Increasing antidumping effect of intestinal pacing with motor-active agents.

The aim was to determine whether cholecystokinin-octapeptide (CCK-OP), bethanechol Cl, or metoclopramide HCl would increase the antidumping effect of intestinal pacing in five dogs with truncal vagotomy and Roux gastrectomy. While recording electrical activity from the conscious animals, the amount of a 100-ml, 25% dextrose gastric instillate emptied in 20 min was determined during control tests, during tests with CCK-OP (500 ng/kg/hr), bethanechol (80 micrograms/kg/hr), or metoclopramide alone (600 micrograms/kg/hr) given intravenously or during tests using combinations of pacing and drugs. In other tests, intraluminal gastrointestinal pressure was measured during control and drug infusions. CCK-OP, which relaxed the proximal stomach, slowed emptying of the dextrose instillates (mean +/- SEM emptied, no pacing, no drug = 74 +/- 5 ml; CCK-OP alone = 34 +/- 5 ml; P less than 0.05). CCK-OP also enhanced the slowing effect produced by pacing (pacing alone = 41 +/- 7 ml; pacing plus CCK-OP = 19 +/- 8 ml; P less than 0.05). In contrast, bethanechol and metoclopramide, which did not alter proximal gastric motility, did not alter emptying or augment or diminish the effect of pacing. The conclusion was that the combination of pacing and CCK-OP slowed gastric emptying of the dextrose more than pacing alone and thus had a greater antidumping effect. In contrast, neither bethanechol nor metoclopramide enhanced the pacing effect.

Action Potentials↗
PubMed1983

Constipation with colonic inertia. A manifestation of systemic disease?

Transit of radiopaque markers was delayed in the ascending colon of 51 females and 3 males treated for severe idiopathic constipation. Onset of symptoms was between age 10 and 20 in more than half of the patients. Eighteen percent had previously undergone unnecessary laparotomy for large bowel pseudoobstruction. Stool frequency ranged from 1 stool every three days to 1 every 2 months. Twenty-six percent suffered from fecal incontinence. In addition, 30% had orthostatic hypotension and 15% galactorrhea of idiopathic origin. Patients had a higher than normal anal pressure (P less than 0.001). They all had a rectoanal inhibitory reflex, but it was abnormal in 76%. In the upper esophageal sphincter, resting pressure was higher (P less than 0.02), and coordination poorer (P less than 0.05) than in normal control subjects. Incidence of spontaneous tertiary contractions in the body of the esophagus was greater than normal (P less than 0.03). In the lower esophageal sphincter, resting pressure was lower (P = 0.001) and gastroesophageal gradient weaker (P = 0.05). Closing pressure of the sphincter was lower (P less than 0.001) and coordination less adequate (P less than 0.02). After subcutaneous injection of 0.035 mg/kg bethanechol, urinary bladder intraluminal pressure increased by over 15 cm H2O in 31% of patients but never did in controls, and average maximal pressure was greater (P less than 0.025). Time taken to reach peak pressure was shorter (P less than 0.01). This study provides evidence that patients who suffer from constipation with colonic inertia also have abnormal function in other hollow viscera.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1981

Effect of oral bethanechol on parameters of esophageal peristalsis.

It has been suggested that enhanced esophageal peristalsis may be an additional reason for the therapeutic effect of oral bethanechol (B) in reflux patients and for the improved acid clearing seen with B. This study was designed to determine the effect of oral B on various parameters of esophageal peristalsis. Healthy young adult males were studied with an intraesophageal transducer assembly. Amplitude, dp/dt, and velocity profiles for the smooth muscle portion of the esophagus were produced. Oral B, 25 mg, produced a significant increase (P less than 0.05) in amplitude in the distal esophagus from 15 to 45 min after drug administration. The effect on dp/dt was similar but not as marked. Oral bethanechol produced decreases in velocity at all points, reaching significance (P less than 0.05) at the most distal measuring site, 30 and 45 min after injection. Oral B produces a stronger but slower, perhaps more efficient, progression of the peristaltic wave in normal humans. Our findings may explain improved acid clearance found with this agent.

Adult↗
PubMed1983

Effect of chronic ethanol feeding on pancreatic enzyme secretion in rats in vitro.

The effect of long-term ethanol intake on pancreatic digestive enzyme secretion was determined in Sprague-Dawley rats. Weight-matched triplets were fed Lieber-DeCarli diet containing 5% w/v concentration of ethanol, isocaloric amounts of Lieber-DeCarli diet, or rat chow ad libitum for 6, 12, and 18 months. Basal and bethanechol-stimulated secretion of amylase, lipase, trypsinogen, chymotrypsinogen, and pancreatic secretory trypsin inhibitor (PSTI) was determined. In the ethanol-fed group, basal secretion of trypsinogen and chymotrypsinogen was increased at 6, 12, and 18 months. In addition, basal secretion of amylase and lipase was increased and that of PSTI was decreased at 12 and 18 months. Secretion of PSTI was stimulated by bethanechol (10(-4)M), whereas the secretion of digestive enzymes was not stimulated in the ethanol-fed versus two control groups. At 12 months the dose-response curve of amylase and lipase secretion was shifted upwards in the ethanol-fed group with increase in ED50. These data are suggestive of membrane perturbations leading to increased basal secretion and a subsensitivity of the cholinergic receptors in the ethanol-fed group. Increased basal secretion of proteases in the presence of diminished trypsin inhibitor indicates that premature activation of proenzymes could occur resulting in pancreatitis.

Amylases↗
PubMed1985

Lidocaine inhibition of esophageal peristalsis and lower esophageal sphincter pressure in baboons.

Intravenous lidocaine was infused at 0.82 ml/min in a concentration of 1.2 mg/ml (2.3 mg/kg) for 120 min in awake chair-restrained baboons (Papio anubis), and measurements of esophageal peristalsis and LES pressure were compared before and after lidocaine or control infusions. Lidocaine produced a progressive and significant (P less than 0.05) decrease in amplitude in the peristaltic wave in the smooth muscle portion of the distal esophagus during the 120-min infusion. Lower esophageal sphincter pressure was similarly significantly lower than control after the infusion of lidocaine (P less than 0.05). Velocity and duration of the peristaltic wave were unchanged during the infusion. The decreased amplitude occurred during therapeutic and stable serum concentrations of lidocaine. It did not appear that the inhibitory effect of lidocaine was due to an induction of prostaglandin synthesis, because pretreatment of animals with indomethacin did not change the inhibitory effect of lidocaine, and serum metabolites of prostacyclin decreased during the infusion. Furthermore, the inhibitory effect of lidocaine was not topical. The response to the muscarinic agonist, bethanechol was similar in lidocaine-treated animals and control animals. The preservation of a bethanechol response after lidocaine inhibition of LES pressure and distal esophageal amplitude suggests that lidocaine acts proximal to the muscarinic receptor in the esophageal body and smooth muscle portion of the lower esophageal sphincter. This study suggests that lidocaine produces an inhibitory effect on the peristaltic wave and lower esophageal sphincter pressure that is similar to inhibitory effects described after anticholinergic agents and calcium channel blocking drugs, but intravenous lidocaine infusion requires a longer period of time to produce inhibition of muscle function.

Animals↗
PubMed1981

Evaluation of elevation of the head of the bed, bethanechol, and antacid form tablets on gastroesophageal reflux.

To ascertain how elevation of the head of the bed, bethanechol, and antacid foam tablets affect gastroesophageal reflux, we used prolonged intraesophageal pH monitoring in 55 symptomatic patients. Acid exposure was separated into reflux frequency and esophageal acid clearance time and recorded during the day in the upright posture and recumbent at night. Values before and during each therapy were compared to physiologic reflux in 15 asymptomatic controls. Ten patients slept with the head of the bed elevated and had a 67% improvement in the acid clearance time (P less than 0.025); however, the frequency of reflux episodes remained unchanged. Twelve patients given 25 mg of bethanechol 4 times a day had a 50% decrease in recumbent acid exposure only (P less than 0.05), due to a trend towards decreased reflux episodes and acid clearance in time. Bethanechol combined with head of bed elevation in 19 other patients decreased both reflux frequency (30%) and acid clearance time (53%, all P less than 0.05). Antacid foam tablets failed to significantly diminish acid exposure. Nocturnal reflux responded the best to those therapies tested.

Antacids↗
PubMed1986

Cholinergic stimulation of human pancreatic secretion.

The effect of graded doses of bethanechol on pancreatic secretion and plasma levels of pancreatic polypeptide and somatostatin was investigated in six healthy volunteers. In other studies the effect of a bethanechol background on the secretin-CCK stimulation of pancreatic secretion was also studied. Bethanechol caused a moderate stimulation of amylase secretion with a weak stimulation of bicarbonate secretion. These effects were not associated with significant changes in the plasma level of pancreatic polypeptide and somatostatin. Bethanechol enhanced the response to secretin and CCK. These results confirm a cholinergic pathway in the stimulation of pancreatic secretion in man.

Adult↗
PubMed1986

Effect of somatostatin on amylase secretion from in vivo and in vitro rat pancreas.

In the present study the effect of somatostatin on amylase secretion was determined using in vivo cannulation and isolated acini from rat pancreas. In vivo somatostatin-14 inhibited amylase secretion in basal state and that stimulated with CCK8 and acetylcholine. Somatostatin-14 and somatostatin-28 failed to inhibit amylase secretion from isolated acini in basal state and that stimulated with CCK8 and bethanechol. Somatostatin-14 did not increase 45Ca uptake or efflux of label from acini preloaded with 45Ca. Cellular cyclic AMP levels were not significantly increased. Somatostatin-14 did not alter the synthesis of proteins in vitro, as judged by incorporation of a mixture of fifteen 14C-labeled amino acids. Somatostatin-14 stimulated phosphoprotein phosphatase in higher doses, whereas no effect was observed at lower doses. Inhibition of secretion in vivo and lack of stimulation of amylase secretion in isolated acini suggest that the somatostatin effect in vivo is mediated by an indirect effect similar to other peptides, for example, opiates and neurotensin. Stimulation of phosphoprotein phosphatase suggests that somatostatin may bind to the acinar cells and affect functions other than secretion and synthesis of enzymes.

Acetylcholine↗
PubMed1981

Evidence for an intestinal mechanism of pancreatic polypeptide release.

The purpose of this study was to define the existence of an intestinal phase of pancreatic polypeptide (PP) release and to assess whether it was mediated by a cholinergic-sensitive mechanism. Four conscious dogs with 20-cm upper intestinal Thiry-Vella loops and chronic gastric fistulas were used. The Thiry-Vella (T-V) loops were perfused with 10% liver extract or 0.154 M NaCl at a rate of 1 ml/min for 120 min. In a separate experiment, 240 ml of 10% liver extract was infused over a 5-min period into the stomach via the gastric fistula. Basal PP levels were 29 +/- 4 fmol/ml. The gastric infusion of liver extract caused a significant increase of plasma PP levels to a peak of 215 +/- 29 fmol/ml (P less than 0.05). The perfusion of the T-V loop with liver extract significantly increased plasma PP levels over basal to a peak of 73 +/- 14 fmol/ml (P less than 0.05). This value was significantly less than that released by gastric infusion of liver extract (P less than 0.05). Perfusion of the loop with NaCl did not significantly alter basal plasma PP levels (P greater than 0.05). PP release by perfusion of the T-V loop with liver extract was abolished by atropine intravenous bolus (0.2 mg/kg). Although the combination of bethanechol (100 microgram/kg/hr intravenous) and liver extract consistently increased the plasma levels of PP, the values did not attain statistical significance when compared to liver extract alone (P greater than 0.05). The data presented are thus consistent with the hypothesis that there is an enteric phase of pancreatic polypeptide release and that this enteropancreatic reflex is mediated by a cholinergic-sensitive mechanism which might be hormonal or neural.

Animals↗
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↗
PubMed1983

GABA-mimetic effect on gastric acid secretion. Possible significance in central mechanisms.

Parenteral administration of beta-(p-chlorophenyl)-gamma-aminobutyric acid (PCP-GABA), a lipophilic GABA mimetic, has been shown to aggravate stress-induced ulcerations in the rat. Since acid hypersecretion may be a possible mechanism for this, we studied the effect of graded doses of PCP-GABA on rat gastric acid secretion. The stimulatory effect of PCP-GABA was found to be dose-dependent, long-acting, and massive, exceeding the maximal effects of histamine and bethanechol. The acid stimulant effect of PCP-GABA was completely abolished not only by atropine but also by truncal vagotomy. Vagotomized, PCP-GABA-treated animals responded to bethanechol, suggesting that a peripheral (cellular) mechanism is not involved. We conclude that PCP-GABA acts centrally to activate vagal centers and to cause acid hypersecretion. Although hypersecretion of acid caused by PCP-GABA may be involved in the observed aggravation of stress-induced ulceration in the rat stomach, evidence for this has yet to be provided.

Animals↗
PubMed1989

Gastrointestinal myoelectric activity in an infant with congenital idiopathic motility disorder.

We investigated myoelectric activity in an 8-month-old male who presented with a perinatal bowel obstruction, duodenal band, congenital short small intestine, and persistent feeding intolerance. Serosal electrodes were surgically implanted on stomach, duodenum, and jejunum during Nissen fundoplication and ileostomy. A 5-cm ileal specimen was taken for in vitro studies. Spontaneous migrating myoelectric complexes (MMC) were present in stomach and small intestine. Bethanechol increased electrical response activity (ERA) in stomach and duodenum. Morphine induced intense ERA and distinct phase III activity. Pentagastrin infusion did not disrupt MMC cycling. Feeding disrupted MMC complex cycling 30-40 min after the meal. Metoclopramide before feeding delayed disruption of the MMC cycling after the feeding. Intermittent gastric arrhythmias were present after the fifth postoperative day. In vitro muscle strips showed spontaneous contractions and electrical control activity (ECA). Bethanechol, McNeil A-343, motilin, and cholecystokinin induced contractions, but pentagastrin had no effect. We conclude that in spite of a major clinical motility dysfunction, several of our findings were normal. The abnormalities include short MMC period, absence of disruption of MMC by pentagastrin, and gastric arrhythmias.

Bethanechol↗
PubMed1988

Effect of various prokinetic agents on post Roux-en-Y gastric emptying. Experimental and clinical observations.

The effect of various prokinetic drugs was assessed in animals with Roux-en-Y gastrojejunostomy. The agents tested were (1) bethanechol 2.5 mg subcutaneously at 0 min and 30 min postprandially (pp); (2) metoclopramide 20 mg intravenous bolus at 0 min pp; (3) a combination of 1 and 2; (4) oxytocin 5 mg intramuscularly at 0 min and 240 min pp; (5) motilin at 100 ng/kg/hr; or (6) 300 ng/kg/hr continuous intravenous infusion from 0 to 270 min pp. Only bethanechol administration resulted in significantly less gastric retention (65 +/- 6% vs 32 +/- 5% retention at 5 hr). (P less than 0.002). The animal results with parenteral bethanechol were confirmed in humans with chronic delayed gastric emptying following Roux-en-Y gastrojejunostomy, with a decrease in gastric retention on radionuclide scan from 78.5 +/- 5% to 26 +/- 12% at 2 hr pp (P less than 0.01). Initially all patients responded with symptomatic improvement. However, subsequently 3/6 (50%) of patients required total or near total gastrectomy for recurrent symptoms of gastric stasis. Nevertheless, 2/6 (33%) of patients have no further evidence of gastric stasis, and a trial of bethanechol is recommended prior to considering further gastrectomy in patients with the Roux-stasis syndrome.

Animals↗
PubMed1988

Role of inflammatory mediators in colonic smooth muscle function in ulcerative colitis.

Patients with ulcerative colitis have a decrease in colonic motility which may increase their diarrheal symptoms. Studies in patients with ulcerative colitis showed that the postprandial spike response was slightly decreased and the intraluminal pressure response was absent. In vitro studies showed that the circular smooth muscle, obtained from patients with ulcerative colitis or from a rabbit model of experimental colitis, generated decreased force compared to muscle not associated with mucosal inflammation. The decrease in muscle contraction was observed with bethanechol stimulation or electrical field stimulation. Since the response to an increased extracellular concentration of potassium [( K+]0) was also diminished, the decreased response appears to be caused by an abnormality in the intrinsic contractile mechanism of colonic smooth muscle. Further studies are necessary to determine if metabolic abnormalities are present in the colonic muscle in patients with colitis.

Animals↗
PubMed1989

Prospective evaluation of high-dose bethanechol in investigation of esophageal chest pain.

We compared the value of bethanechol 80 micrograms/kg subcutaneously, acid infusion with a 0.1 normal hydrochloric acid, and edrophonium 80 micrograms/kg intravenously as provocative agents to reproduce chest pain and manometric alterations in 72 patients with noncardiac chest pain. No patient developed typical chest pain and manometric alteration with acid infusion, while five (6.9%) patients developed these changes with edrophonium and four (5.6%) with bethanechol. Only one patient developed diagnostic changes exclusively with bethanechol. All patients tested with bethanechol developed some degree of local pain or significant cholinergic symptoms, with two patients requiring atropine for relief. Side effects from edrophonium were infrequent (28% of patients tested) and did not require atropine administration. We conclude that, using the parameters of typical chest pain and the development of manometric alterations as proof of the esophageal origin of chest pain, bethanechol at 80 micrograms/kg adds little information beyond that obtainable with edrophonium. Further, the high incidence of bethanechol-related side effects at 80 micrograms/kg suggests that this dose should not be generally recommended.

Bethanechol↗