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 73 records · Page 4Linked to original sources
PubMedDate not supplied

Hepatic microvascular regulatory mechanisms. II. Cholinergic mechanisms.

Several cholinergic agonists and their antagonists were administered topically at various concentrations (10(-10) to 10(-4) gm per ml) to the livers of anesthetized Sprague-Dawley rats. Changes in the microvasculature were measured for a period of 15 min using in vivo microscopic methods. The influence of cholinergic agonists on hepatic mast cells was determined by histochemical methods. Cholinergic agonists elicited constriction of portal venules, sinusoids, and terminal hepatic (central) venules accompanied within 5 to 20 sec by the adherence of platelets and leukocytes to the endothelial lining of these vessels. These responses were not observed in hepatic arterioles or hepatic (sublobular) venules. However, the responses drastically altered cellular flow through all segments of the microvasculature. The drugs were effective in the following ranking: bethanechol greater than pilocarpine greater than carbachol. Vascular responses were not antagonized by atropine; phentolamine modified the constrictor response of portal venules but of no other microvascular segment. These results suggest that the responses were not mediated by cholinergic (muscarinic) receptors and that the constriction of portal venules was caused by the chemical activation of alpha-adrenergic receptors. Histochemical methods revealed that pilocarpine and bethanechol also elicited a significant decrease in the number of visible mast cells suggestive of degranulation and the release of serotonin, histamine, and other polyanions (e.g., heparin) from these cells. Release occurred within the same period of time as the microvascular alterations (15 min.). These data provide additional evidence that mast cell constituents and adrenergic mechanisms are involved in hepatic cholinergic mechanisms.

Animals↗
PubMed1989

Effect of metoclopramide, bethanechol, and loperamide on gastric residence time, gastric emptying, and mouth-to-cecum transit time.

The effects of metoclopramide, bethanechol, and loperamide on the gastric residence time (GRT), gastric emptying (GE), and mouth-to-cecum transit time (MCTT) of a solution were investigated in three separate studies of five healthy male volunteers each. Metoclopramide in doses of 5, 10, and 15 mg prolonged GRT by 33, 88, and 162%, respectively, almost reaching statistical significance (p 0.058). A relationship was observed between GRT prolongation, and metoclopramide area under the plasma-time curve (p 0.01) and metoclopramide observed time to maximum concentration (p 0.01). Metoclopramide had an inconsistent effect on MCTT. Bethanechol 50 mg prolonged GRT by 64% (p 0.031) and had no effect on MCTT. Loperamide at doses of 2 and 8 mg prolonged GRT by 18 and 115% (p 0.043) and MCTT by 30 and 130% (p 0.0001), respectively. None of these motility-altering agents affected GE.

Adolescent↗
PubMed1992

Bethanechol inhibition of chicken intestinal brush border Na/H exchange: role of protein kinase C and other calcium-dependent processes.

Bethanechol, a muscarinic agonist, inhibits the initial rate of amiloride-sensitive Na uptake by intact mucosa of avian small intestine as well as by isolated chicken villus enterocytes, an effect that is maximal at 90 seconds and reverses by 6 minutes. Bethanechol similarly decreases intracellular pH in isolated cells suspended in bicarbonate-free buffer in a time course similar to inhibition of enterocyte Na uptake, suggesting inhibition of Na/H exchange. In brush border membrane vesicles rapidly prepared from cells stimulated with bethanechol, proton-dependent 22Na uptake is transiently inhibited in a time course similar to inhibition of cell Na uptake. Bethanechol also stimulates transient translocation of protein kinase C from the cytosol to the particulate fraction, a portion of this activity translocating to the brush border membrane. To determine the calcium dependence of bethanechol's action, enterocytes were loaded with varying concentrations of the calcium buffering agent quin-2. Inhibition of cell Na uptake by the calcium ionophore ionomycin could be completely reversed by quin-2 buffering in a concentration-dependent manner. In contrast, quin-2 buffering had little or no effect on the inhibition of Na uptake caused by the protein kinase C activators phorbol esters and oleoylacetylglycerol. Bethanechol's inhibitory effects were partially, but not completely reversed by quin-2 buffering. These data suggest that the effects of bethanechol on chicken villus enterocyte brush border Na/H exchange are mediated by calcium-dependent process(es) as well as by protein kinase C.

Animals↗
PubMed1975

Technique for assessment of local effects of substances found in bile upon opening pressure of choledochoduodenal junction.

An assessment of the localized influences of various chemicals found in bile was made by applying them to the interior of the canine choledochoduodenal junction. Test agents were isolated by air bubbles and introduced into the terminal lumen of the intramural portion of the common bile duct via the pressure measurement catheter; they remained in the duct for approximately 1.5 min. The system was flushed and opening pressures were then measured. Responses were measured in terms of alterations in ductal opening pressures generated by a linear pressure ramp. Histamine, serotonin, and bethanechol markedly increased ductal opening pressures, whereas epinephrine and norepinephrine decreased opening pressures. None of the agents affected either cardiovascular or small intestinal motor activity in the vicinity of the sphincter when administered in the manner. The results suggest that the presence in bile of certain neurohumoral transmitters and neurohumoral-like agents may directly affect the canine choledochoduodenal sphincter function.

Animals↗
PubMed1987

A complication of the Infusaid pump: duodenal atony reversed by urecholine.

The totally implantable infusion pump (Infusaid pump) for treating metastatic disease to the liver is a new treatment that is gaining widespread acceptance. However, as might be expected for any new major surgical procedure, there are increasing reports of complications. We report a complication in which duodenal atony was caused by the infusion of the chemotherapeutic agent (FUDR) into the stomach and duodenum. The atony was totally reversed by the subcutaneous administration of urecholine.

Bethanechol Compounds↗
PubMed1993

Effects of atropine, glucagon, and bethanechol on urodynamics of continent cecal urinary reservoir before and after complete, partial, and sham detubularizations in dog.

Effects of muscarinic receptor blockade (atropine), stimulation (bethanechol), and bowel smooth muscle relaxant (glucagon) on the urodynamics of the continent cecal urinary reservoir in a tube form and after complete, partial, and sham detubularizations were studied using dogs. Complete detubularization significantly increased capacity and decreased spontaneous motor activity, whereas the other types of detubularization had no significant effects on them. Neither atropine nor glucagon had influence on the basal pressure, but they increased the capacity and the volume at which the first pressure wave appeared and decreased the wave amplitude. After detubularization glucagon further decreased uninhibited contractions while atropine totally abolished them. The highest capacity and lowest motor activity was gained when atropine or glucagon was given in cases with detubularized pouch demonstrating an additive effect of the detubularization and drug. Also, bethanechol increased the motor activity and decreased the volume in detubularized problem in a patient with a detubularized cecal pouch, orally administered anticholinergic or bowel smooth muscle relaxing drugs may be useful in management.

Animals↗
PubMed1993

Effect of partial outlet obstruction on choline acetyltransferase activity in the rat and rabbit.

Partial outlet obstruction of the rabbit bladder induces a rapid and significant increase in bladder mass. This increase in mass is associated with a variety of specific contractile dysfunctions, characterized by a marked decrease in the response to field stimulation (acting through the release of neurogenic transmitters). There is histological evidence indicating that the decrease in the contractile response of isolated strips of rabbit urinary bladder to field stimulation is associated with a degeneration of synaptic membranes within the bladder detrusor (neuropathy). In the current experiments, the effect of partial outlet obstruction in rabbit and rat urinary bladders on choline acetyltransferase activity (ChAT) were determined and correlated with both the level of bladder hypertrophy (increase in mass) and the contractile response to field stimulation. The results can be summarized as follows: In the rabbit, partial outlet obstruction induced a rapid 5-fold increase in bladder mass over the 7 day period of study. This increase in mass was associated with a decrease in the contractile response of isolated strips of bladder body and base to field stimulation and a decrease in ChAT activity. Interestingly, the rabbit bladder base showed a significantly higher ChAT activity than the bladder body, although the contractile response to muscarinic stimulation was significantly greater in the bladder body than in the base. In the rat, partial outlet obstruction induced a mild 2-fold increase in bladder mass.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Effect of partial outlet obstruction on contractility: comparison between severe and mild obstruction.

Detrusor dysfunction is one of the most common problems in patients with outflow obstruction secondary to benign prostatic hyperplasia. These patients complain of various symptoms, including urinary frequency, urge incontinence, difficulty in voiding, and retention. The severity of the symptoms is dependent on the stage of disease and/or severity of the obstruction. We compared the changes in the rat detrusor function following both mild and severe models of partial outlet obstruction in the rat. Outflow obstructions were created by ligation of the urethra over which a catheter was placed. The size of the catheter determined whether the severity of obstruction was mild or severe (1.70 mm for mild obstruction and 1.09 mm for severe obstruction). Changes in the bladder weight, length-tension relationships, and the contractile response to field stimulation, pharmacologic agonists, and KCl were studied in bladders isolated from 1 and 2 week obstructed rats. Bladder weights of all obstructed rats increased significantly. The weight of the severe obstructed rats were significantly greater than rats subjected to mild obstruction. In general, passive length-tension curves of obstructed rats were shifted to right. The magnitude of the active tension induced by high KCl was higher in the mild obstruction and lower in the severe obstruction. The maximum response to KCl of mild obstruction was generated at greater lengths than for the other groups. In general, the contractile responses of the mild obstructed bladder body to field stimulation, bethanechol, KCl, and ATP, and of the bladder base to field stimulation, KCl, and methoxamine, were significantly increased when compared to the responses of the control bladder body and base. However in the severe obstructed bladder, the responses to field stimulation, KCl, ATP, and methoxamine were significantly reduced from the responses of the control strips; the response to bethanechol was similar for control and the severe obstructed groups. In conclusion, the severity of outlet obstruction significantly altered the contractile response of the bladder. Mild obstruction induced a mild increase in bladder mass, which was associated with significant increases to all forms of stimulation. Severe outflow obstruction induced a substantial increase in bladder mass and a significantly greater reduction in the response to field stimulation than the response to bethanechol (which was unchanged).

Adenosine Triphosphate↗
PubMed1993

Distribution and function of the adrenergic and cholinergic receptors in the fetal calf bladder during mid-gestational age.

Previous studies on the developing fetal bovine bladder demonstrate that compliance is low during early stages of fetal development and increases with fetal age. In addition, the pharmacological response of isolated fetal bovine bladder smooth muscle strips to field stimulation and bethanechol increased in proportion with the gestational age. In the adult bladder (rabbit), the contractile response to autonomic receptor stimulation and the autonomic receptor density showed a parallel gradation in the the bladder between bladder dome and the urethra. The present studies were designed to determine the distribution of the cholinergic and adrenergic receptors in the urinary bladder of the fetal calf at mid-gestational age, and to correlate the receptor density with the magnitude of the response to receptor stimulation. Each bladder body was separated into upper, middle, and lower segments. For the functional studies, circular and longitudinal strips were cut from each bladder segment and stimulated with field stimulation (FS), bethanechol, methoxamine, isoproterenol, and KCl. Autonomic receptor assays were performed using 3H-QNB (muscarinic cholinergic), 3H-DHE (alpha adrenergic), and 3H-DHA (beta adrenergic) as ligands. In general, there were no significant differences in receptor density among the three bladder segments. However, the density of muscarinic receptors was significantly greater than the density of alpha- or beta-adrenergic receptors for all bladder segments. The receptor densities correlated very well with the functional response of isolated bladder strips to the specific autonomic agonists. The contractile response of isolated bladder strips to the specific autonomic agonists. The contractile responses of the strips to FS, bethanechol, and methoxamine were not significantly different among the three different bladder segments.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Effect of altering smooth muscle tone on maximal expiratory flows in patients with tracheomalacia.

We obtained maximal partial expiratory flow-volume (PEFV) curves using the rapid compression technique in three infants with intrathoracic tracheomalacia. Maximum flows were quantitated at functional residual capacity (VmaxFRC). Studies were performed at baseline, after inhalation of methacholine (MCh) and after inhalation of albuterol. At baseline, all three patients had significantly lower than normal VmaxFRC values, and two patients displayed expiratory flow limitation during tidal breathing. VmaxFRC improved significantly after MCh administration, but fell back toward or below baseline after albuterol. Additionally, the ratio of forced to tidal flows at mid-tidal volume (Vmid(forced/tidal), a reflection of expiratory flow reserve, increased after MCh administration and decreased after albuterol. Two patients also received oral bethanechol: 2.9 mg/M2, q 8 hr for 10 days, after which PEFV curves were repeated. Both Vmax FRC and Vmid(forced/tidal) were increased over baseline after bethanechol administration, but decreased after albuterol. These results suggest that in patients with abnormally collapsible tracheae, stimulation of tracheal smooth muscle can improve airway stability, thereby increasing forced expiratory flows. Additionally, relaxation of airway smooth muscle by bronchodilators can have the opposite effect and exacerbate obstruction.

Albuterol↗
PubMed1990

Effect of bladder outlet obstruction on the morphology, physiology, and pharmacology of the bladder.

Bladder outlet obstruction secondary to benign prostatic hyperplasia induces numerous changes in bladder morphology, physiology, and pharmacology. These changes have been studied experimentally in various animal models, and while each species has advantages and disadvantages, it is unclear which is most like man. It has been shown that tissue hypertrophy leading to an increase in tissue mass develops rapidly after bladder outlet obstruction. Ischemia induced by the obstruction results in acute muscle dysfunction. The degree of functional impairment is directly related to the degree of tissue hypertrophy. However, the bladder contractile apparatus appears to have a surprising regenerative ability, such that recovery of bladder function becomes obvious 14 days after obstruction. Urodynamic changes include an increase in urinary frequency and voiding pressure and a decrease in voided volume. Clinically, involuntary bladder contractions are often present. Determination of which of these specific aspects of outlet obstruction the investigator is interested in studying will dictate the selection of the most appropriate animal model.

Animals↗
PubMed1993

Peptide YY inhibits pancreatic secretion via cholinergic pathways.

The influence of extrapancreatic nerves and intrapancreatic cholinergic activity on the inhibition of pancreatic exocrine secretion by peptide YY (PYY) was studied in conscious dogs. Chronic pancreatic fistulae were created in five mongrel dogs while a second group of five dogs also underwent complete pancreatic denervation. After recovery, a continuous infusion of secretin (62 ng/kg/hr) and cholecystokinin (50 ng/kg/hr) was administered over 2 hr. An infusion of PYY (400 pm/kg/hr) was then given randomly, during either the first or second experimental hour. The experiments were then replicated with a continuous background infusion of (90 micrograms/kg/hr) bethanechol, a cholinergic agonist. The secretin/cholecystokinin-induced bicarbonate and protein outputs were significantly inhibited by PYY in both the innervated and denervated animals. In the denervated animals, bethanechol eliminated the inhibitory effects of PYY. We conclude that extrapancreatic nerves do not mediate the inhibitory effects of PYY. The results suggest that PYY inhibits secretin/cholecystokinin-induced pancreatic response by an intrapancreatic cholinergic mechanism.

Animals↗
PubMed1989

Inhibition of the contraction of the isolated longitudinal muscle of the guinea-pig ileum by botulinum C2 toxin: evidence for a role of G/F-actin transition in smooth muscle contraction.

The effect of botulinum C2 toxin was studied on the contractions of the guinea pig ileum myenteric plexus longitudinal muscle preparation. Botulinum C2 toxin inhibited the muscle contraction induced by electrical stimulation (60 V; 0.5 ms; 0.33 Hz) in a time and concentration dependent manner. The inhibitory effect occurred with a time lag of about 1 h, and depended on the presence of both toxin components. After 4 h of incubation with 1.7 micrograms/ml of component I and 6.7 micrograms/ml of component II of botulinum C2 toxin, the smooth muscle contraction was inhibited by about 60%. At these toxin concentrations, about 55% of the modifiable smooth muscle actin was ADP-ribosylated. Smooth muscle contraction induced by bradykinin and bethanechol were similarly inhibited. Moreover, the C2 toxin inhibited muscle contraction induced by Ba2+, and by direct muscle membrane depolarization (60 V; 10 ms; 0.33 Hz) after suppression of acetylcholine release by normorphine. Also cytochalasin D inhibited the electrically evoked contraction of the ileum longitudinal muscle. In contrast to botulinum C2 toxin, inhibition of contractility by cytochalasin D occurred without a lag phase, and was reversed by washing off the toxin. In contrast of guinea pig ileum longitudinal muscle, botulinum C2 toxin did not reduce the contraction of the rabbit aortic smooth muscle stimulated by K+-depolarization or noradrenaline.

Actins↗