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PubMed1993

Nortriptyline in the hospitalized elderly: tolerance and side effect reduction.

This article describes two separate but related studies regarding the use of nortriptyline (NT) in the treatment of depressed elderly inpatients. The first study assesses medication tolerance to NT during the acute treatment of late-life depression. The second describes a placebo-controlled study of the effect of bethanechol in reducing antimuscarinic side effects of NT. Antidepressant pharmacotherapy was considered for 72 patients with late-life depression; 17 (24%) did not receive NT; 5 (7%) because of absolute or relative medical contraindications. Of the 55 patients who started on NT, 9 percent had side effects that necessitated medication discontinuation. A separate sample of 26 elderly depressed patients being treated with NT participated in a double-blind, placebo-controlled trial of bethanechol. Patients receiving bethanechol had reduced subjective complaints of anticholinergic side effects and showed improvement on an objective measure of salivary flow.

Aged↗
PubMedDate not supplied

The effect of glucagon on cholinomimetic responses of the recto-sigmoid.

Motor activity of the lower bowel was induced by the parenteral administration of prostigmine or bethanechol in 7 subjects. Intraluminal pressure recordings from the sigmoid colon and rectum revealed that the augmented responses of motor activity to these cholinomimetic drugs were similar both in duration and in motility indexes. The intravenous administration of glucagon inhibited the motor responses to both cholinomimetic stimuli employed. A possible mechanism for the inhibitory action of glucagon is suggested and the clinical application of these observations is discussed.

Adult↗
PubMed1977

The lower esophageal sphincter as a barrier to gastroesophageal reflux.

UNLABELLED: To correlate lower esophageal (LES) pressure and gastroesophageal (GE) reflux, esophageal manometry and GE scintiscanning have been used to study 40 consecutive patients. Serial scintiscanning was performed as the GE pressure gradient was increased in increments. Reflux was calculated from the ratio of esophageal to gastric radioactivity. The relationship between GE reflux and LES pressure was inverse (r = 0.60, P less than 0.005). Two subgroups of 10 patients were studied further. After atropine, LES pressure decreased from 11.2 +/- 1.1 to 5.3 +/- 0.9 mm Hg (P less than 0.01) at 20 min. The GE reflux index increased from 8.3 +/- 2.1 to 13.4 +/- 2.2% (P less than .05). After bethanechol, LES pressure increased from 8.9 +/- 0.8 to 18.5 +/- 1.0 mm Hg (P less than 0.001) at 30 min. GE reflux decreased from 11.9 +/- 2.4 to 5.8 +/- 1.7% (P less than 0.01). CONCLUSIONS: first, GE reflux correlated with basal LES pressure by an inverse relationship; second, atropine decreased LES pressure and increased reflux; third, bethanechol increased LES pressure and decreased reflux. These data suggest that LES pressure is an important determinant of GE competence.

Atropine↗
PubMed1977

Afterdischarge on postganglionic sympathetic nerves following repetitive stimulation of the preganglionic nerve to the rat superior cervical ganglion in vitro.

An asynchronous firing or afterdischarge (AD) was recorded in vitro from the postganglionic internal carotid nerve of the rat superior cervical ganglion following repetitive stimulation of the preganglionic nerve when ganglion transmission was blocked by chlorisondamine, nicotine or hexamethonium, but was rarely observed in untreated ganglia. A stimulus frequency of at least 5 Hz was required to induce AD and as few as 100 pulses caused a significant response. The amplitude and duration of AD varied with the number of pulses. Low calcium solutions resulted in AD in the absence of ganglion blocking drugs, and high calcium solutions or low concentrations of atropine abolished the AD. Increasing magnesium concentration to 10 mM or the manganese concentration to 0.1 mM reduced or prevented AD following preganglionic nerve stimulation. The onset of AD was delayed in potassium-free solutions and at a lowered temperature. Dinitrophenol had a small depressant effect on AD but sodium azide reduced the amplitude significantly. Exposure of ganglia to bethanechol, 300 to 600 muM, resulted in asynchronous firing recorded from postganglionic nerves, and stimulation of the preganglionic nerve transiently depressed the drug-induced firing but enhanced the firing 30 to 60 seconds after the volley. Physostigmine did not alter the amplitude of bethanechol-induced firing after a volley. Prolonged high frequency (40 Hz) stimulation of the preganglionic nerve increased the AD following a 20 Hz test volley for up to 1 hour. It is concluded that increasing the release of acetylcholine or blockade of nicotinic receptors makes more acetylcholine available for interaction with muscarinic receptors, and that stimulation of the preganglionic nerve unmasks or sensitizes ganglionic muscarinic receptors. No clear evidence of a metabolic basis for the muscarinic response was obtained.

Animals↗
PubMed1977

Effect of secretin on myoelectrical and mechanical activity of the isolated canine stomach perfused ex vivo.

Totally isolated whole canine stomachs, perfused ex vivo with homologous blood, were used for recording of myoelectrical and mechanical activity prior to and following the injection of secretin. Secretin was given as flash injections (0.5 - 32 U) or constant infusions (60 U/h). Background stimulation of stomachs was obtained by intragastric instillation of fluid, by the infusion of pentagastrin or bethanechol chloride, and by electrical stimulation of the Latarjet branch of the vagus nerve. Hormones were injected into the gastric arterial circulation. Secretin had no effect on the frequency of electrical control activity. Secretin inhibited electrical response activity when injected against the background of electrical vagus stimulation. Secretin also inhibited or decreased mechanical activity of the gastric antrum, recorded at the site of the antral strain gauge.

Action Potentials↗
PubMed1977

The occlusive competence of the duodenal orifice of the canine pancreatic duct.

Observations by scanning electron microscopy indicate that the mucosa of the terminal part of the major pancreatic duct of the dog is organized into numerous, highly convoluted folds. The individual mucosal cells are tall, columnar and studded with numerous microvilli. These folds are highly vascularized. The intraluminal administration of bethanechol and norepinephrine is associated with subsequent increases and decreases of mean opening pressures. Mean opening pressures were not observed to be associated with autonomic nervous activity that was unaccompanied by changes in systemic arterial pressure. It is concluded that the terminal portion of the canine major pancreatic duct probably acts as a passive valve, the occlusive competence of which is influenced by the status of the vasculature of the lining mucosa in this region.

Animals↗
PubMed1977

Symptomatic diffuse esophageal spasm. Manometric follow-up and response to cholinergic stimulation and cholinesterase inhibition.

Uniform criteria for defining symptomatic diffuse esophageal spasm (SDES) are lacking. Records of patients undergoing esophageal motility studies over a 3-year period were reviewed. Those patients who fulfilled a predefined set of arbitrary criteria for SDES returned for repeat motility study. Manometric abnormalities seen on initial examination remained unchanged on follow-up evaluation. In addition, response in SDES to two pharmacological agents--a cholinergic agonist and cholinesterase inhibitor--was evaluated and compared to that seen in normal subjects and in subjects with heartburn. Patients with SDES responded similarly to both agents, and their responses were significantly greater than those seen in controls or in subjects with heartburn. The results suggest that SDES is a relatively homogenous entity, with respect to both maintaining stability of manometric abnormalities and response to two different pharmacological agents. The future evaluation of similarly defined patients may lead to ascertaining more clearly the underlying pathophysiology of this "syndrome".

Adult↗
PubMed1995

Role of endogenous nitric oxide in the control of exocrine and endocrine pancreatic secretion.

L-Arginine (L-Arg), that is a substrate for nitric oxide (NO) synthase, stimulates the release of pancreatic islet hormones but the mechanism of this stimulation is unknown. The aim of this study was to determine the role of NO in the control of endocrine and exocrine pancreatic secretion in response to sham feeding (SF), ordinary meat feeding (F), duodenal perfusion with nutrients and i.v. infusion of gastrin releasing peptide (GRP) or urecholine in conscious dogs with chronic pancreatic fistulas. SF1 F, duodenal nutrient and GRP and urecholine resulted in the stimulation of pancreatic secretion reaching, respectively, 50%, 50%, 40%, 85% and 20% of maximal response to caerulein (200 pmol/kg-h i.v.). Infusion of L-Arg (50 mg/kg + 5 mg/kg-h i.v.) almost doubled the basal pancreatic protein secretion and significantly increased the secretory response to SF, F, and duodenal nutrient. After i.v. administration of L-NNA (2.5 mg/kg + 0.5 mg/kg-h), an inhibitor of NO synthase, the pancreatic secretory responses to SF, F, duodenal nutrient, GRP and urecholine were significantly inhibited by about 74%, 70%, 70%, 80% and 30%, respectively. When L-Arg was combined with L-NNA, the reduction in pancreatic secretion induced by L-NNA was significantly attenuated. SF resulted in a marked rise in plasma insulin and glucagon and this response was completely abolished by L-NNA infusion. Insulin and glucagon levels were 2-3 folds increased by F and L-NNA infusion inhibited these responses while the addition of L-Arg partly reversed this inhibition. Duodenal nutrient produced several fold increase in plasma insulin and glucagon levels that were significantly reduced by L-NNA and this reduction was partially reversed by L-Arg. GRP also caused moderate rise in plasma insulin and glucagon levels which were significantly reduced by L-NNA and this was partially restored by L-Arg. We conclude that SF, F, duodenal nutrient, GRP or urecholine stimulate both the exocrine and endocrine pancreatic secretion and that these effects are mediated, at least in part, through the NO pathway.

Animals↗
PubMed1996

Potentiation by baclofen of gastric acid secretion stimulated by secretagogues in vagotomized rats under anesthesia.

The effect of intravenous administration of baclofen, a GABA(B) receptor agonist, on gastric acid secretion from perfused stomach was studied in vagotomized rats anesthetized with urethane. Baclofen did not stimulate acid secretion by itself. In contrast, baclofen dose-dependently potentiated acid secretion induced by pentagastrin, bethanechol and direct vagal stimulation, but not by histamine. Baclofen-potentiated acid secretion induced by pentagastrin and bethanechol was not influenced by pretreatment with atropine or cimetidine, respectively. Baclofen-potentiated acid secretion evoked by direct vagal stimulation was prevented by pretreatment with proglumide which is a gastrin receptor antagonist. Baclofen-potentiated acid secretion evoked by bethanechol was partly prevented by bicuculline methiodide which is a GABA(A) receptor antagonist, but not by phaclofen which is a GABA(B) receptor antagonist, suggesting an involvement of peripheral GABA(A) receptors. Baclofen-potentiated acid secretion induced by direct vagal stimulation was not affected by the change of body temperature. These results suggest that baclofen stimulates acid secretion under certain conditions, and that two mechanisms are involved in this effect. The effects of baclofen on acid secretion may be mediated by increasing the release of histamine by pentagastrin, bethanechol and direct vagal stimulation. In addition, baclofen would also be effective if muscarinic agents were already occupying muscarinic acetylcholine receptors on parietal cells.

Anesthesia↗
PubMed1977

Acinar cell responsiveness to urecholine in the rat pancreas during fetal and early postnatal growth.

These studies were performed to determine when, during fetal or postnatal life, rat pancreatic acinar cells acquire their capacity to respond to cholinergic drugs. The release of amylase, lipase, and chymotrypsin from rat pancreas in response to urecholine was measured in vitro. Fetal and newborn pancreas did not respond to 10(-5) M urecholine; 3-day- to 15-day-old pancreas demonstrated an increasing response to this dose. Peak sensitivity when compared to adult pancreas was present between days 15 and 21. Our results indicate that the exocrine pancreas acquired a responsiveness to urecholine on the 3rd day of postnatal life and becomes more sensitive to stimulation from the 15th day.

Amylases↗
PubMed1977

[Therapy of gastroesophageal reflux].

In spite of numerous experimental and clinical studies the pathogenesis of the disease resulting from pathological gastroesophageal reflux is yet unsettled. The importance of hiatus hernia has been questioned. The disturbed function of the lower esophageal sphincter does not always explain the occurrence of increased gastroesophageal reflux. there is no correlation between symptoms (pyrosis) and the typical esophageal mucosal changes which are best demonstrated by means of endoscopy. Guided biopsy is usually not necessary. Medical therapy consists in application of antacids, most effectively in combination with alginic acid. Further help can be expected from stimulation of the lower esophageal sphincter with metoclopramide and/or cholinergic drugs. Further measures are elevation of the head of the bed (30 degrees), reduction of body weight if necessary (to reduce intraabdominal pressure) and a high protein, low fat diet. Operative intervention (fundoplicatio) is rarely indicated, mostly in case of stricture.

Antacids↗
PubMed1976

In vitro dog detrusor strip contractile responses and calcium ion activity.

In vitro detrusor strip experiments show that the presence of calcium ion is essential for spontaneous and bethanechol-induced detrusor contractile activity. 45Ca uptake experiments show that detrusor strips subjected to bethanechol show increased 45Ca uptake with significant decrease in total muscle strip calcium. There is a significant increase in the percentage of calcium exchange, suggesting that calcium efflux has exceeded influx. Kinetic analysis of 45Ca uptake by detrusor strips shows more 45Ca to reside in the slow component of strips following exposure to bethanechol. This suggests that calcium associated with bethanechol-induced contractile activity comes to occupy intracellular or more tightly bound membrane sites.

Animals↗
PubMedDate not supplied

Pharmacological analysis of the abomasum-rumen reflex in sheep.

Contractions of the dorsal sac of the rumen and abomasum were recorded in the sheep with chronic fistulae. It was found that during reflex inhibition of rumen contractions, induced with stimulation of chemoreceptors in the abomasum, an increased sympathicotonia plays an essential role and the beta-adrenergic receptors mediate the reflex.

Abomasum↗
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 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↗
PubMed1976

Influence of histamine releasing agents on gastric acid secretion of isolated bullfrog gastric mucosa.

The influence of histamine releasing agents on gastric acid secretion was studied in isolated bullfrog gastric mucosa preparations. Maximum acid secretory responses in our preparations were obtained by stimulation with tetragastrin (5 X 10(-7) g/ml), histamine (1 X 10(-5) g/ml) and bethanechol (1 X 10(-6) g/ml). Compound 48/80 (1 X 10(-4) g/ml) showed a transient stimulatory action which was followed by a gradual depression of basal acid secretion. The stimulatory phase of compound 48/80 was completely antagonized by burimamide (1 X 10(-5) g/ml), a histamine H2-receptor antagonist. In gastric mucosa preincubated with compound 48/80, the secretagogue action of tetragastrin or bethanechol was not exerted, although this preparation continued to respond to histamine. The effects of Triton X-100, decylamine and polymixin B were quite similar to those of compound 48/80. After pretreatment with compound 48/80, the gastric mucosa preparation became refractory to the stimulatory action of compound 48/80 or Triton X-100. It is thus suggested that endogenous histamine may play an important role in the secretagogue action of tetragastrin and bethanechol.

Animals↗
PubMed1998

An assessment of two gastric transport models currently used in safety pharmacology testing.

1. The potential effects of new drugs on the digestive system can be examined in a number of model systems of which intestinal motility in the mouse and/or gastric emptying in the rat are examples recommended for safety pharmacology evaluation. 2. Intestinal motility, assessed by the transit of carmine dye in the mouse and gastric motility, assessed by stomach weight in the rat, were examined using a range of clinical drugs or potent pharmacological agents known to affect gastrointestinal function. Assessment of both models in the guinea-pig was also evaluated. 3. Activity was demonstrated with codeine, diazepam, atropine and CCK-8 (all of which inhibited gastric function). However, neither model gave consistent and reliable results with the remaining reference compounds, namely metoclopramide, bethanechol, cisapride, deoxycholate, carbachol and domperidone. 4. In conclusion, this investigation questions the usefulness of simple models of gastrointestinal transport in the rodent as a means of detecting potential effects of a new drug on the digestive system. This finding should be of concern to the pharmaceutical industry as these simple models are routinely used as part of a regulatory safety pharmacology 'package' of studies.

Animals↗