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At least 163 records · Page 9Linked to original sources
PubMed1985

Direct cerebrospinal fluid infusion of bethanechol chloride in Alzheimer's disease: use of an implantable continuous infusion device.

Recently, investigation into an experimental treatment for patients with Alzheimer's disease has begun utilizing surgical implantation of a continuous infusion device to deliver a muscarinic agonist, bethanechol chloride, directly into the cerebrospinal fluid (CSF). The nurse research assistant has been very active in this study being involved in patient evaluation, preoperative and postoperative patient education, collection of data, and refill of the infusion device. The neurosurgical nurse also plays an active role in patient education, immediate preoperative and postoperative care, and careful observation and recording of patient behavior and general well-being. Success of continued research based on this protocol will be enhanced by the contributions of the nurse research assistant and neurosurgical nurse familiar with the study and with her/his anticipated role.

Activities of Daily Living↗
PubMedDate not supplied

Metoclopramide enhances bethanechol-induced pancreatic exocrine secretion of the dog.

The effects of metoclopramide on pancreatic exocrine secretion were investigated in the pentobarbitone-anaesthetized dog. All drugs were injected into the femoral vein. Metoclopramide (10-1000 micrograms/kg) did not change the resting rate of pancreatic secretion. Pancreatic secretion, induced by bethanechol (3 micrograms/kg), was dose-dependently enhanced by simultaneous injections of metoclopramide (10 and 30 micrograms/kg), but the protein and bicarbonate concentrations of the pancreatic juice were not affected. Secretions induced by secretin (0.1 units/kg) and dopamine (3 micrograms/kg) were not modified by metoclopramide at up to 30 micrograms/kg. A larger dose of metoclopramide (1000 micrograms/kg) suppressed dopamine-induced secretion to a lesser extent than the same dose of sulpiride. From these results, it is concluded that metoclopramide enhances secretory responses to cholinergic stimulations by peripherally sensitizing the muscarinic receptor-mediated exocrine process and this drug is a weaker antagonist of the dopamine D2 receptors than sulpiride.

Animals↗
PubMed1988

Intracerebroventricular bethanechol chloride administration in Alzheimer's disease.

In June 1983 we began evaluating intracerebroventricular (ICV) cholinergic drug infusion in patients with biopsy-documented Alzheimer's disease (AD). An initial trial in four patients showed this treatment approach to be feasible, but objective improvement in cognitive or social function was not documented. A double-blind, placebo-controlled crossover study involving a larger number of patients has since been done. The results of this study, presented here, document a statistically significant improvement in some neuropsychological test results during periods of drug infusion. However, the degree of improvement is not sufficient to justify further treatment with the presently available drug, bethanechol chloride.

Aged↗
PubMed1993

The effect of terodiline on hyperreflexia (in vivo) and the in vitro response of isolated strips of rabbit bladder to field stimulation, bethanechol and KCL.

Hyperreflexia, a condition characterized by contractions of the urinary bladder, is not mediated by a micturition reflex. The contractions can be of neurogenic origin through spinal or supraspinal reflexes or of myogenic origin, independent of neuronal mediation. There is a clear relationship between hyperreflexia and symptoms such as urgency, frequency, nocturia and urinary incontinence. Therapies to reduce the presence of uninhibited bladder contractions include oral drug therapy, instillation drug therapy and parasympathetic nerve ablation. The current study characterizes the ability of terodiline to inhibit an experimental form of hyperreflexia and compares the efficacy and potency of terodiline and other agents on hyperreflexia and evoked contractions. The results can be summarized as follows: (1) terodiline inhibits the amplitude of the hyperreflexia at lower concentrations than it inhibits the frequency of hyperreflexia; (2) terodiline had no statistically significant effect on mean blood pressure at any concentration utilized; (3) terodiline had approximately the same potency for inhibition of 2 and 32 Hz stimulation for both the bladder body and base; (4) terodiline inhibited the maximum contractile response to bethanechol and also shifted the curve to the right, demonstrating that terodiline is a mixed inhibitor, and (5) terodiline was a noncompetitive inhibitor of KCl.

Animals↗
PubMed1983

Gastric bicarbonate secretion in humans. Effect of pentagastrin, bethanechol, and 11,16,16-trimethyl prostaglandin E2.

Although the stomach is mainly known for its ability to secrete hydrochloric acid, there is increasing evidence that the gastric mucosa also secretes bicarbonate. A simple method for simultaneous measurement of gastric HCO-3 secretion and H+ secretion was developed from a two-component model of gastric secretion. The method, which is based upon gastric juice volume, H+ concentration, and osmolality, was validated both in vitro and in vivo. In 14 healthy human beings, basal gastric HCO-3 secretion averaged 2.6 mmol/h (range, 0.7-8.7 mmol/h). Basal HCO-3 secretion was approximately 50% of basal H+ secretion and there was a significant correlation between basal HCO-3 and H+ secretion in individual subjects (r = 0.79). HCO-3 was secreted in basal nonparietal secretion at a concentration of approximately 90 mmol/liter. Intravenous pentagastrin infusion markedly stimulated H+ secretion but did not increase HCO-3 secretion. During pentagastrin infusion, the cholinergic agonist, bethanechol, significantly augmented H+ secretion (from 20.2 to 24.7 mmol/h) and increased HCO-3 secretion (from 2.2 to 4.2 mmol/h). A prostaglandin E2 analogue significantly reduced H+ secretion and increased HCO-3 secretion during pentagastrin infusion. The reduction in net gastric juice H+ output following prostaglandin E2 was due more to H+ secretory inhibition than to HCO-3 secretory stimulation. We conclude that the healthy human stomach actively secretes HCO-3 and that gastric HCO-3 secretion can be influenced by cholinergic stimulation and by prostaglandin E2.

Adult↗
PubMed1988

Bethanechol chloride as a suggested adjunct to prolonged in vivo exposure therapy in the treatment of paruresis.

A major difficulty in treating paruresis (psychogenic urinary retention) by prolonged in vivo exposure therapy involves the individual's inability to initiate urination in response to anxiety-provoking stimuli easily and frequently enough to generalize the desired behavior to everyday situations. Administration of bethanechol chloride, a parasympathomimetic compound that facilitates urination by prompting contraction of the detrusor muscle of the bladder, prior to therapeutic sessions is suggested to enhance the efficiency and effectiveness of in vivo desensitization procedures in the treatment of paruresis.

Behavior Therapy↗
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↗
PubMed1990

[Efficacy of combination of Ea-0643 (bunazosin hydrochloride) and bethanechol chloride in patients with neurogenic bladder].

Bethanechol chloride, a cholinergic agent and bunazosin hydrochloride, an alpha adrenergic blocking agent were administered orally to 28 patients with neurogenic bladder due to peripheral nerve disorders. To compare the effect of the two drugs, one of the drugs was initially administered orally for 2 weeks, and then both of them were administered for the next 2 weeks. Since there were some significant differences in the patient background between the two groups, it was difficult to compare the two drugs. However combined use of these drugs resulted in both objective and subjective good responses in those patients.

Adrenergic alpha-Antagonists↗
PubMed1983

Anticholinergic potency of diphenhydramine (Benadryl) measured against bethanechol in the gastric fistula dog.

We quantitated the gastric secretory anticholinergic effect of diphenhydramine (Benadryl) against graded doses of bethanechol, a cholinergic agonist, which was used to stimulate acid and pepsin secretion. Anticholinergic potency of diphenyhydramine was 10,000 times less than that reported for atropine and was 1,000 times less than the reported potency of diphenhydramine antagonism of histamine H-1 effects.

Animals↗
PubMed1983

Modification of pancreatic carcinogenesis in the hamster model. 7. Inhibitory effect of bethanechol chloride.

Experiments were designed to investigate in the hamster model the effect on pancreatic carcinogenesis of bethanechol chloride (BC), which is known to increase pancreatic protein synthesis in rats. Hamsters received a single (15 mg/kg body weight) dose of BC either before, simultaneously with, or after a single dose of N-nitrosobis(2-oxopropyl)amine (BOP; 20 mg/kg body weight). A second group was treated daily with BC (7.5 mg/kg body weight) for 24 weeks, following BOP. The control groups consisted of animals treated with BOP only, with BC only, and with solvent only. The surviving hamsters were killed 46 weeks after BOP treatment. BC, whether given before, simultaneously with, or after BOP, significantly reduced the incidence of pancreatic ductal/ductular carcinomas. The multiplicity, size, and latency of carcinomas were also affected by BC. A more pronounced inhibition of cancer induction occurred in the group treated daily with BC after BOP. The possible mechanisms involved in the inhibitory action of BC on pancreatic carcinogenesis are discussed.

Animals↗
PubMed1983

[The bethanechol test in the diagnosis of neurogenic bladder. 60 cases].

Bethanechol denervation hypersensitivity test seems useful although sometimes disregarded, for the diagnosis of lower neurogenic bladder. Our own experience of 60 patients is presented. When the indications are good (large capacity, hypotonic bladder, clinical suspicion of lower neuron lesion) and when the interpretation is based on a right understanding of its mechanism, this test appears to be very reliable. Except in 4 cases, the difference of pressure is greater than 20 or less than 10 cm H20. Factors susceptible to interfere with its accuracy are summarized. We must admit some discrepancies between the results of this test (exploring the pelvic nerve) and the perineal EMG (exploring the pudendal nerve); this fact is illustrated here. The importance of a wide bladder neck as a radiologic sign of neurogenic bladder is also stressed.

Bethanechol↗
PubMed1988

Effect of metoclopramide, bethanechol and the cholecystokinin receptor antagonist, L-364,718, on gastric emptying in the rat.

The prokinetic effects of metoclopramide, bethanechol and L-364,718 on a semisolid meal and solid pellet gastric emptying were evaluated and compared. Each compound increased the rate of meal emptying as measured 90 min post-dose. L-364,718, a non-peptide CCK antagonist, was the most potent of these three agents with statistically significant activity observed at 0.03, 0.1 and 0.3 mg/kg p.o. Only metoclopramide significantly enhanced pellet emptying in a dose-dependent manner (3-30 mg/kg p.o.). The effects of each test agent and the potential physiologic role of cholecystokinin in regulating gastric emptying are discussed.

Animals↗
PubMed1980

Gastrin release after truncal vagotomy in fistula dogs: hypersensitivity to bombesin but not bethanechol.

Integrated gastrin response was measured by the serial changes in serum immunoreactive gastrin after various stimuli in three dogs with gastric fistula and highly selective fundic vagotomy, who were then subjected to truncal vagotomy. Truncal vagotomy eliminated the gastrin as well as the gastric acid response to vagal excitation by 2-deoxy-glucose, but did not significantly changes the responses to bethanechol (20 or 120 micrograms/kg/hr by IV infusion). Acid output was the same with bombesin or its nonapeptide in the dogs with fundic vagotomy as it was after subsequent truncal vagotomy, but gastrin release was very much increased by truncal vagotomy. For a 3-hour infusion of bombesin integrated gastrin release was 65 and 143 ng/ml/min and for its nonapeptide 43 and 109 ng/ml/min in the dogs with fundic and truncal vagotomy respectively. The marked hypersensitivity of the gastrin response after truncal vagotomy to bombesin but not to a cholinergic agonist suggests that the antral denervation led to a post-denervation hyper-response to the putative transmitter, bombesin, and that the vagal release of antral gastrin may thus represent a peptidergic neurohormonal mechanism. Also, a long half-life of effect suggests that bombesin binds avidly to its receptors.

Animals↗
PubMed2004

Antinociceptive effects of bethanechol or dimethylphenylpiperazinium in models of phasic or incisional pain in rats.

The mechanism by which muscarinic or nicotinic agonists produce antinociception has been the subject of several studies. In the present investigation, we used intrathecal administration of drugs to rats to show that muscarinic or nicotinic agonists such as bethanechol (BCh) and dimethylphenylpiperazinium (DM), respectively, dose-dependently increased the tail flick latency and reduced the pain produced by a surgical incision performed on the plantar aspect of a hind paw. The effects of BCh in both tests were inhibited by the previous intrathecal administration of atropine, but not mecamylamine (muscarinic and nicotinic antagonists, respectively). Mecamylamine significantly reduced the effects of DM in both tests. Atropine significantly reduced the effect of DM in the tail flick test and inhibited the effect of DM against the incisional pain. Intrathecal hemicholinium-3 (HC-3), a reversible inhibitor of choline transporter, did not change the effect of BCh in the tail flick test but produced a non-significant reduction of the effect of BCh against incisional pain. In contrast, HC-3 produced a non-significant reduction of the effect of DM in the tail flick test but fully inhibited the effect of DM against incisional pain. Therefore, the BCh-induced antinociception depends on a direct activation of muscarinic receptors, whereas DM-induced antinociception results in drug interaction with nicotinic receptors to activate the further release of acetylcholine from intrinsic spinal cholinergic terminals. The acetylcholine released by DM in turn induces antinociception via activation of muscarinic receptors.

Acetylcholine↗
PubMed1980

The effects of bethanechol chloride on urodynamic parameters in normal women and in women with significant residual urine volumes.

A 5 mg. subcutaneous dose of bethanechol chloride was given to 12 women with residual urine volumes equal to or greater than 20 per cent of bladder capacity but no evidence of neurologic disease, or anatomic or functional outlet obstruction and to 27 normal women wtih approximately the same mean age. The cystometric and some profilometric parameters did change, indicating that the drug was pharmacologically active. No improvement in voiding function was noted, as judged by residual urine volume and flow rate measurements. These results raise significant questions regarding the contemporary use of this drug, especially in the currently recommended oral dosages.

Bethanechol Compounds↗
PubMed1976

Dyssynergic vesicourethral responses during bladder rehabilitation in spinal cord injury patients: effects of suprapubic percussion, credé method and bethanechol chloride.

Five normal men and 70 spinal cord injury male patients underwent 100 studies with the multiple pressure recording technique, incorporating the continuous infusion principle for sphincter pressure monitoring. Gross cystosphincteric dyssynergia was noted in the majority of patients with complete upper motor neuron bladders less than 2 years in duration. Some form of synergic voiding patterns was noted, mostly in patients with incomplete upper motor neuron bladders. The external sphincter tends to be synergic in late cases of upper moto neuron bladders. Internal sphincter dyssynergia is uncommon in cases of injuries less than 2 years in duration, with the exception of patients who have autonomic dysreflexia. Bladder neck obstruction seems to be more common in late lesions secondary to global hypertrophy of the bladder. Rehabilitation maneuvers and bethanechol chloride administration may exaggerate detrusor sphincter dyssynergia and injudicious use of such procedures could be detrimental to the urinary tract.

Adult↗