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At least 1,189 records · Page 66Linked to original sources
PubMed1982

Dysfunction of the detrusor and urethra in multiple sclerosis: the role of drug therapy.

Urinary tract disorders secondary to multiple sclerosis are common. In this series of 24 patients with multiple sclerosis, 5 had normal function of the detrusor, 3 had detrusor hypotonicity and 16 had detrusor hyperreflexia. The proximal urethra was evaluated using radiologic and electromyographic techniques. These studies showed that 5 patients had a normal urethra, 15 had some degree of somatic dyssynergia and 3 had sympathetic dyssynergia. Detrusor hyperreflexia with somatic dyssynergia was found in 11 patients and was the most common pattern. The therapeutic response to standard pharmacologic preparations was also evaluated. The regimen was based on the clinical and urodynamic findings for each patient. Dicyclomine hydrochloride was the drug of choice for detrusor hyperreflexia, bethanechol chloride for hypotonicity, dantrolene sodium for somatic dyssynergia and phenoxybenzamine hydrochloride for sympathetic dyssynergia. The authors found that most of their patients were amenable to drug therapy, the exception being those with advanced neurologic lesions.

Adult↗
PubMed1982

Effect of isosorbide and hydralazine in painful primary esophageal motility disorders.

Five patients with painful primary esophageal motility disorders underwent pharmacologic testing with isosorbide and hydralazine. While neither agent affected baseline amplitude or duration of distal esophageal contractions, pretreatment with hydralazine significantly blunted the response to bethanechol (mean esophageal contraction duration, 31.4 +/- 4.8 s after bethanechol alone vs. 12.7 +/- 1.8 s after bethanechol and hydralazine p less than 0.005). Premedication with isosorbide was significantly less effective. In addition, while all 5 patients experienced chest pain in response to bethanechol alone, only 1 of 5 experienced chest pain in response to bethanechol after previous hydralazine administration; 3 patients had chest pain after previous administration of isosorbide. Patients who were placed on long-term oral hydralazine therapy experienced improvement in chest pain and dysphagia with concomitant decrease in amplitude and duration of esophageal contractions on repeat motility study (176.5 +/- 23.8 mmHg to 97.3 +/- 27.0 mmHg, p less than 0.05, 7.5 +/- 0.8 s to 5.2 +/- 0.5 s, p less than 0.005). Hydralazine appears to be of value in the treatment of diffuse esophageal spasm and other painful primary esophageal motility disorders.

Adult↗
PubMed1982

Interdigestive motor activity in patients with systemic sclerosis.

Fasting antral, duodenal, and jejunal motor activity and plasma motilin and pancreatic polypeptide were studied in 14 patients with systemic sclerosis, 6 and 9 without clinical evidence of small bowel involvement, and 8 healthy control subjects. Normal interdigestive motor activity was present in control subjects and patients without intestinal involvement. However, cyclic motor activity was absent in 3 of the patients with intestinal disease and the motility index per interdigestive cycle (or per 6-h recording period in those without cyclic activity) was significantly less in the antrum (181 +/- 103 mm2 compared with 760 +/- 86 and 1116 +/- 96 mm2 for patients without involvement and healthy control subjects, respectively), duodenum (153 +/- 101 mm2 compared with 1425 +2- 186 nd 1055 +/- 241 mm2), and jejunum (268 +/- 131 mm2 compared with 1166 +/- 97 and 1105 +/- 128 mm2). Metoclopramide and bethanechol significantly increased motor activity at the three sites in all subjects but the magnitude of the metoclopramide response was less in patients with intestinal involvement. Fasting concentrations of motilin and pancreatic polypeptide exhibited cyclic variation with peak values occurring during phase 3 of the interdigestive cycle. Plasma motilin during each phase of motor activity was significantly higher in patients with scleroderma, with or without intestinal involvement, than in control subjects. The abnormal motor activity demonstrated here indicates a possible mechanism by which intestinal stasis and bacterial overgrowth could occur and by which clinical disturbances of intestinal transit might arise.

Adult↗
PubMed1982

Giant hypertrophic gastropathy (Ménétrier's disease): pharmacologic effects on protein leakage and mucosal ultrastructure.

Seven patients with giant hypertrophic gastropathy participated in a gastric intubation perfusion study to investigate the route and mechanism of protein leakage associated with this disease. All patients had gastric tight junctions wider than those in healthy controls. Acute administration of propantheline bromide reduced gastric albumin leakage (-50.7%, p less than 0.05) and concurrently decreased width of tight junctions (p less than 0.05) in all patients. Another antisecretory agent, cimetidine, had no consistent effect on protein leakage or on the width of tight junctions. Pentagastrin and bethanechol chloride increased protein loss but had no effect on the width of tight junctions. These results are consistent with the hypothesis that proteins may take a paracellular route via the tight junctions as they traverse the gastric mucosa and that this may have a cholinergic mechanism.

Adult↗
PubMed1982

Bethanechol or cimetidine in the treatment of symptomatic reflux esophagitis: a double-blind control study.

We conducted a double-blind study to compare the effectiveness of oral bethanechol chloride or cimetidine in treating reflux esophagitis to evaluate the drugs' effects on the symptoms of esophagitis and its verification by endoscopy. Forty-three patients were treated with either 300 mg of cimetidine or 25 mg of bethanechol chloride, each administered four times a day for six weeks. In addition to this drug treatment, the patients all received conventional medical therapy. Patients who were treated with either of the two drugs experienced a decrease in symptoms and less severe endoscopic lesions. While cimetidine treatment resulted in complete endoscopic healing in 15 of 22 patients, bethanechol treatment resulted in the same healing in 11 of 21 patients. During therapy, neither endoscopic lesions or symptoms worsened. Our study indicated that either cimetidine or bethanechol is an effective drug in treating reflux esophagitis. The effects of the two drugs can be favorably compared.

Administration, Oral↗
PubMed1982

Cholinergic stimulation of immunoglobulin A secretion in rat intestine.

This study was undertaken to assess a possible role for cholinergic agents in the regulation of intestinal immunoglobulin A secretion. Intestinal loops, constructed in anesthetized rats, were perfused with phosphate buffered normal saline. Immunoglobulin A concentrations were measured by radioimmunoassay. When compared with the effect of normal saline in the same rats, intravenous injection of pilocarpine, 10 mg/kg, increased immunoglobulin A concentrations in perfusates from ileal loops (p less than 0.001). Qualitatively similar results were obtained with muscarine and bethanechol, from jejunal and colonic loops, and from unanesthetized rats. Immunoglobulin A concentrations increased four- to eightfold during maximal cholinergic stimulation. Atropine, 250 micrograms intravenously, completely blocked the effect of pilocarpine on immunoglobulin A secretion (p less than 0.005), and also inhibited basal intestinal immunoglobulin A secretion for 40 min after injection. As determined on 10%-40% sucrose density gradients, much of the immunoglobulin A secreted after cholinergic stimulation sedimented in the 11S range. These data indicate that intestinal secretion of immunoglobulin A is stimulated by the muscarinic effect of cholinergic agonists, and suggest that basal secretion of immunoglobulin A may be influenced by the parasympathetic nervous system.

Anesthesia, General↗
PubMed1982

Muscarinic receptors on rat isolated colonic epithelial cells. A correlation between inhibition of [3H]quinuclidinyl benzilate binding and alteration in ion transport.

Muscarinic cholinergic agonists stimulate secretion or inhibit absorption in the large intestine both in vivo and in vitro, effects that are completely inhibited by atropine, a specific muscarinic antagonist. These studies were performed to determine if the muscarinic-induced alteration in electrolyte transport in rat colon was produced by muscarinic agonists binding directly to receptors on colonic enterocytes. We found that crude membranes prepared from rat isolated colonic epithelial cells had a specific, saturable, high affinity receptor for L-[benzilic-4,4-3H]quinuclidinyl benzilate, a potent muscarinic antagonist with an apparent dissociation coefficient of 0.56 +/- 0.11 nM and a maximum number of binding sites of 42.5 +/- 5.7 fmol/mg protein. Muscarinic antagonists inhibited L-[benzilic-4,4-3H]quinuclidinyl benzilate binding in nanomolar concentrations, and muscarinic agonists inhibited L-[benzilic-4,4-3H]quinuclidinyl benzilate binding in micromolar concentrations. In parallel studies, oxotremorine and bethanechol, muscarinic agonists, and racemic quinuclidinyl benzilate altered short-circuit current in rat colon in vitro in concentrations that were in good agreement with the concentrations that inhibited L-[benzilic-4,4-3H]quinuclidinyl benzilate binding to the crude membrane preparation. Thus, these studies demonstrate that the muscarinic-induced alteration in colonic electrolyte transport is directly related to agonist binding to a specific muscarinic receptor on the colonic epithelial cell.

Animals↗
PubMed1982

Both nicotinic and muscarinic agonists acutely increase tyrosine 3-monooxygenase activity in the superior cervical ganglion.

The activity of tyrosine 3-monooxygenase in rat superior cervical ganglia in vitro was measured by monitoring their rate of dopa production. Cholinergic agonists produce a rapid and reversible increase in dopa synthesis in the ganglia. Carbachol (0.1 mM) causes a 5- to 6-fold increase in dopa synthesis. The action of carbachol is largely inhibited by the nicotinic antagonist hexamethonium (3 mM) and is completely blocked by a combination of hexamethonium and the muscarinic antagonist atropine (6 microM). Dimethylphenylpiperazinium (1 mM), a specific nicotinic agonist, produces a 4-fold increase in dopa synthesis. The action of dimethylphenylpiperazinium is blocked by hexamethonium but not by atropine. Bethanechol (1 mM), a muscarinic agonist, causes a 2-fold increase in dopa synthesis. The action of bethanechol is inhibited by atropine but not by hexamethonium. It is concluded that tyrosine 3-monooxygenase activity in rat superior cervical ganglia can be increased by both nicotinic and muscarinic stimulation, that nicotinic stimulation can produce a greater increase than can muscarinic stimulation and that carbachol increases enzyme activity by a combination of both pathways. These cholinergic mechanisms for the acute regulation of tyrosine 3-monooxygenase may be activated in vivo by acetylcholine released from preganglionic neurons and thus may play a role in the physiological regulation of catecholamine synthesis in sympathetic ganglia.

Animals↗
PubMed1982

Pirenzepine inhibits acid and pepsinogen secretion by the isolated perfused mouse stomach.

Acid and pepsinogen secretion were studied in the isolated luminally perfused mouse stomach. Stimulation was obtained with bethanechol 10(-5)M. Pirenzepine blocked the effect of bethanechol in a dose dependent manner. The minimal blocking dose was 10(-5)M. Atropine 10(-6)M blocked secretion to a similar extent as pirenzepine 10(-5)M. Addition of tetrodotoxin did not change the response to bethanechol or to bethanechol together with pirenzepine. It is concluded that acid and pepsinogen secretion stimulated by bethanechol are inhibited by atropine and pirenzepine. There is at present no evidence that bethanechol stimulation or antimuscarinic inhibition act via intramural nerves.

Animals↗
PubMed1982

Acquired postganglionic cholinergic dysautonomia: case report and review of the literature.

An 8-year-old girl with acute abdominal pain had cholinergic autonomic dysfunction. There have been only four patients with acquired postganglionic cholinergic dysautonomia described in the literature. The characteristic clinical features are atony of the bowel and bladder, lack of tears, saliva, and sweat, internal ophthalmoplegia, and normal adrenergic functions. Special studies for autonomic nervous function help in confirming this diagnosis. The exact pathogenesis of the disorder is still not clear. This case demonstrates successful treatment with bethanechol chloride.

Autonomic Nervous System Diseases↗
PubMed1982

In vitro effect of acetylcholine and bethanechol on the contractions of the human detrusor muscle. Influence of prostaglandins.

The effects of acetylcholine and bethanechol on the basal resting tone of the isolated detrusor muscle were explored. It was observed that the tone was augmented by both agents. On the other hand, in the presence of prostaglandin (PG)-inhibitors the dose-response curve of acetylcholine shifts to the right. PGF 2 alpha (10(-10)M) but not PGE2 (10(-10)M) completely blocked the inhibitory effect of PG-inhibitors upon the inotropic effect of acetylcholine, without modifying the influence of bethanechol. After inhibitors of PG-synthesis, eserine abolished the inhibitory action of acetylcholine but did not change the influence of bethanechol. Our results suggest that endogenous PGs facilitate the action of acetylcholine through an increase in the concentration of the cholinergic neurotransmitter probably via an inhibition of the acetylcholinesterase activity.

Acetylcholine↗
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↗