SEARCH · Search PubMed
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.
A review of the management of neurogenic bladder dysfunction in the adult is presented. The various modes of therapy are classified according to their effects on bladder contractility and outlet resistance, providing a logical framework for discussion.
Oxybutynin chloride (Ditropan), a tertiary amine possessing anticholinergic and papaverine-like, direct muscular antispasmodic effects, has been used in controlled clinical studies in patients with neurovesical reflex activity, uninhibited bladders, enuresis, and primary muscle spasm. The cystometrically documented, synergistic, anticholinergic, and muscle relaxant activity of oxybutynin observed in these studies indicates that the drug can be highly effective in the management of reflex neurovesical dysfunction, enuresis, and bladder spasm.
Representative case summaries of patients with different types of neurogenic bladder diagnosed by combined cystometric-perineal electromyography and treated with bethanechol (Urecholine) are presented. Determination of the activity of the periurethral striated muscle in relation to bladder dysfunction is extremely important in the selection of patients for bethanechol therapy. In the absence of structural obstruction, bethanechol can be used in patients with (1) the early phase of coordinated reflex neurogenic bladder and sphincter when there is incomplete bladder emptying due to feeble or unsustained detrusor contractions, (2) recovery phase of spinal shock when the periurethral striated muscle has recovered and is under voluntary control, (3) incomplete motor paralytic bladder with coordinated sphincter, and (4) sensory paralytic bladder with decompensation. The bethanechol regimen will vary in accordance with the type of bladder being treated.
A double blind balanced Latin-square study was conducted on 20 adult patients with decompensated bladders to determine the relative effectiveness of oral and parenteral bethanechol chloride (Urecholine) on the stretch response of bladder muscle. Detrusor reaction was measured by modified cystometry. Five mg. of subcutaneous bethanechol chloride produced a significant increase in intravesical pressure which was more rapid in onset, of larger magnitude, and of shorter duration than oral doses of 100 and 200 mg.
Various parasympathomimetic drugs are discussed, including the choline esters, bethanechol, carbachol, methacholine chloride, and furtrethonium. Other cholinomimetic agents include muscarine, muscarone, arecholine, and pilocarpine. Anticholinesterase agents inhibit or inactivate acetylcholinesterase enzyme and thus result in a prolonged stimulation of cholinergic receptors by endogenous ACh. Bethanechol is the most widely used parasympathomimetic drug in the United States. Its action is mainly muscarinic with activity largely confined to the urinary bladder and to a lesser degree the gastrointestinal tract. It can be administered only subcutaneously or orally, and adequate dosage is necessary for a successful response.
The anticholinergic and antispasmodic activity of atropine, propantheline, imipramine, and flavoxate were judged by each drug's ability to inhibit bethanechol chloride and barium chloride-induced canine detrusor contractions. In this in vitro model, atropine and propantheline are pure anticholinergic agents. Imipramine significantly decreases both bethanechol and barium-induced contractions, while flavoxate only minimally inhibits the response to either stimulant.
Explore the source record for details and available documents.
Using urodynamic testing, vesical dysfunction in patients with multiple sclerosis can be classified and basic therapeutic principles outlined. Satisfactory voiding patterns can be achieved in most patients with multiple sclerosis without surgical procedures. Flexibility and willingness to change programs as the disease process changes make possible reasonably satisfactory results.
Explore the source record for details and available documents.
Sixteen female patients with colonic inertia and 12 control women underwent manometric evaluation of their bladder and rectal cavities. After subcutaneous injection of 0.035 mg./Kg. bethanechol, bladder intraluminal pressure increased by over 15 cm. water in 5 patients (31 per cent) and in none of the control group; maximal pressure after injection was 11.5 +/- 1.6 cm. H2O (mean +/- SE) in patients and 8.5 +/- 1 in controls (p less than 0.025). The intraluminal rectal pressure reached 23 +/- 4 cm. H2O in patients and only 11.9 +/- 1.4 in controls (p less than 0.0025). Time taken to reach a peak pressure was faster in patients both in bladder (17.4 +/- 0.7 vs. 19.8 +/- 1.2 minutes; p less than 0.01) and in the rectum 914.6 +/- 0.8 vs. 16.3 +/- 1.2; p less than 0.025). These findings and the clinical presentation suggest an autonomic neuropathic lesion in this group of patients.
Twelve female and 8 male healthy volunteers underwent urorectodynamic evaluation. Mean bladder capacity was 594 ml. and mean maximal vesical pressure 12.5 cm. water (H2O). Maximal bladder pressure correlated significantly with maximal mural tension (r = 0.96) but did not correlate well with bladder capacity (r = 0.20). Mean bladder volume at first desire to void was 32 per cent of mean bladder capacity. The bladder volume at the first desire did not correlate significantly with the capacity. Mean bladder pressure at 100 ml. volume was 2.9 +/- 0.4 cm. H2O (X +/- SEM). After bethanechol injection, the bladder pressure at 100 ml. volume increased by 8.8 +/- 1.2 cm. H2O (X +/- SEM) at twenty minutes. In only 1 subject did bladder pressure rise higher than 15 cm. H2O (5 per cent). Rectal pressure increased from 1.4 +/- 0.3 to 14.1 +/- 2 cm. H2O (X +/- SEM) at sixteen minutes. Electromyogram (EMG) of the external and sphincter did not follow regular pattern with vesical filling or attempt of voiding. The data obtained in these normal subjects may serve as a basis for comparison in the interpretation of data obtained in patients.
The effect of autonomic active agents were studied on 23 anesthetized cats. The parameters recorded were circular and longitudinal urethral muscles, and bladder muscle contractions and relaxation as well as intravesical pressure during voiding cycles. Cholinergic stimulant (bethanechol) and blockage (atropine) excited or inhibited the bladder muscle and minimally affected the urethra. Alpha-adrenergic stimulant (norepinephrine) in nonatropinized animals produced mild stimulation on the bladder, and longitudinal-circular urethral muscle synergia appeared to be inadequate. In atropinized animals norepinephrine produced the reverse effect, causing marked inhibition. Alpha blockade (phentolamine) disinhibited the receptors mainly in the bladder and improved the urethral synergia. Beta stimulant (isoproterenol) inhibited the bladder and urethral muscles, and beta blockade (propranolol) stimulated the bladder and urethral muscles.
A positive bethanechol supersensitivity test (BST) usually indicates neuropathic detrusor areflexia and warrants neurologic correlation. Seven females, average age thirty-three years, with straining to void and high residual urines, had detrusor areflexia, with a borderline or positive BST, ranging from 19 cm water to 55 cm H2O change in intravesical pressure after 5 mg of subcutaneous bethanechol. However, all patients had a normal neurologic workup, even though 2 patients had insignificant spina bifida occulta. Two of the patients also had prior pelvic surgery, 1 of whom was azotemic, and 4 of the patients had psychosocial problems; factors reported to be associated with a false positive BST. The positive BST is not diagnostic of neurogenic detrusor areflexia because of the many variables that can influence the test. Therefore, the bethanechol supersensitivity test should be interrupted in light of the complete neurourologic evaluation.
The urodynamic results in 68 females with urinary retention were reviewed. There were two groups: 39 patients with neurologic causes for retention, and 29 patients in whom possible causes for retention included: psychological history (15 patients), gynecologic pathology, and urinary tract infection. Nine patients in the neurogenic group and 13 patients in the non-neurogenic group had undergone urethral dilatation with no improvement. Upper urinary tract evaluation was unremarkable. Detrusor failure was the prominent bladder pattern in both groups. In the neurogenic group, low pressure detrusor activity was also present in 10 patients, 3 of whom had sphincter dyssynergia. Flow rate, surface electromyography, and bethanechol supersensitivity test could not help differentiate neurogenic from non-neurogenic detrusor failure. The notation of abnormal bladder sensation did significantly differ between the groups, but was of limited accuracy as an indicator of neurogenic retention. Self-intermittent catheterization was the most effective treatment for both groups, with some patients voiding adequately in follow-up. Although no one test can accurately differentiate neurogenic from nonneurogenic female urinary retention, careful neurourologic evaluation will help guide us to more appropriate management.
Bethanechol has been shown to produce a pharmacologic effect on the urinary bladder, although the clinical efficacy of this response is controversial. The measured response has been an increase in detrusor pressure, although sensory effects may occur also. In this study, 10 neurologically intact men had cystometry before subcutaneous administration of 5 mg bethanechol chloride and thirty minutes after bethanechol. The sensation of desire to void and the maximum cystometric capacity occurred at a higher intravesical pressure and a smaller bladder capacity following bethanechol. Subcutaneous bethanechol appears to alter the bladder pressure and capacity at which the perception of desire to void and the sensation of maximum fullness occurs.
Intraluminal esophageal manometry with a sleeve catheter was used to compare the magnitude of decrease in lower esophageal sphincter (LES) pressure produced by an arterial or venous infusion of prostaglandin E1 in cats. Arterial PGE1 produced significantly lower LES pressures than venous PGE1 (p less than 0.05). Maximal decrease of 75% in basal LES pressure occurred with an associated 15% decrease in systolic blood pressure. The site of action of PGE1 in producing LES hypotension was studied by injection of either edrophonium, or bethanechol during the maximal PGE1 effect. Bethanechol, which acts directly on sphincteric smooth muscle, produced an increase in LES pressure during both saline and PGE1 infusion, while the increases in LES pressure seen with edrophonium during saline infusion were blocked during the PGE1 infusion. From these studies, we conclude that PGE1 produces LES hypotension in the cat by an inhibitory effect on the cholinergic pathway responsible for maintaining LES tone. These studies pharmacologically reproduce the LES pressure abnormality previously reported in the cat during acid-induced esophagitis and support the hypothesis that PGE1 may be involved in the pathogenesis of acute acid-induced lower esophageal sphincter abnormalities.
To investigate the causal relationship, if any, between gastric PG formation and gastric acid output, the release of PGE2 into gastric juice has been studied in eight beagle dogs with a gastric fistula, using sustained half-maximal stimulation by bethanechol and pentagastrin, and in eight duodenal ulcer patients, using the combined sham feeding/pentagastrin test. Immunoreactive PGE2 was determined by a method validated by gas chromatography-mass spectrometry and PGE2 values were normalized by expressing them as ng PGE2 released per meq H+ secreted. In the dogs "steady state" PGE2 output (0.4-10 ng/meq H+) was interrupted during continuous i.v. pentagastrin infusion by symmetrical peaks (50-60 minutes of duration) with a maximum of 24 +/- 3.1 ng/meq H+ (mean +/- SEM). During bethanechol stimulation the rhythmic variations were smaller, but the median values for the periods 30 to 180 or 240 minutes significantly (p less than 0.01) higher (3.9-46 ng/meq H+) than in pentagastrin experiments (0.8-20 ng/meq H+). In humans the peak PGE2 output during sham feeding (3.4-41 ng/meq H+) was significantly (p less than 0.02) larger than following bolus stimulation (6/micrograms/kg) by pentagastrin (2.2-18 ng/Meq H+). The findings are consistent with the hypothesis that activation of muscarinic receptors represents the physiologic mechanism by which gastric release of PGs is regulated. Cyclic variations in gastric PG formation appear to occur in response to vagal stimulation since the peaks in PGE2 output were preceded by increased myoelectrical activity (i.e. mean contractile index).
The effects of drug treatment and of cold-restraint stress (a method used to produce experimental stomach ulcers) on gastric emptying of a resin (colestipol-phenol red complex) were investigated in rats. Gastric emptying was decreased by intraperitoneal treatment with atropine (0.3 mg/kg) or verapamil (4 mg/kg), and enhanced by bethanechol (1.2 mg/kg). Stress by restraint at 4 degrees C for 2 hr markedly reduced gastric emptying; the pattern of effects of drug pretreatment in these stressed rats was similar to that seen in their nonstressed controls. Further experiments, with stress for 3 hr, revealed that the gastric emptying rate was triphasic; increasing in the first hr, returning to normal and then slowing in the third hr of stress. Initial increase in emptying rate was probably due to predominant vagal overactivity. Hypothermia and possibly other factors induced by cold-restraint stress could have subsequently depressed gastric motility.