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Thread: Is drug dangerous

  1. #1
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    Is drug dangerous

    I was prescribed Dicyclomine for abdominal cramps (IBS) is there any thing this drug can do to a nuerogenic bladder?

    The doctor is a GP.

  2. #2
    Super Moderator Sue Pendleton's Avatar
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    http://www.gicare.com/pated/dicyclomine.htm

    I use Levsin and a scoop a day (in water ) of Cholestryamine for my IBS. The Levsin sounds like Dicyclomine. Both are anti-choloregenics (sp?). In other words, like ditropan and detrol they can reduce bladder spasms along with other smooth muscle movements such as bowel and in large doses the heart. If you are doing CIC or use an indwelling catheter you probably won't have a problem. If you rely on "kicking off" and use a condom catheter I'd check back to see what the nurses or Dr Young say.

    Courage doesn't always roar. Sometimes courage is the quiet voice at the end of the day saying, "I will try again tomorrow."

  3. #3
    as mentioned, if you're a spontaneous (reflex) voider, levsin can give you problems since it turns your bladder off

    if you cath, it's just another med to turn off the bladder

  4. #4
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    Its Brand name is Bentyl.

  5. #5
    Cris - dicyclomine is a medication to be used with caution. It can contribute to urinary retention or hesitancy, constipation, dry mouth related to dehydration, and increased risk for hyperthermia (elevated temp). This med can also have several cardiac risks.

    I am not familiar with its use in SCI. Let me check with the SCI team and post their reply. I would urge you to use caution until I can provide further information for you. Do you have a SCI doctor? Another option would be to contact him and discuss the use of this medication and its possible effect/interaction with any other meds that you may be taking. CRF

  6. #6
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    Let me check with the SCI team and post their reply.

    please do

  7. #7
    Cris, it would be of interest to see if it can reduce your bladder spasticity. In theory, it should because it is an anticholinergic drugs. I found several references regarding the drug and bladder:


    • Alberts P (1995). Classification of the presynaptic muscarinic receptor subtype that regulates 3H-acetylcholine secretion in the guinea pig urinary bladder in vitro. J Pharmacol Exp Ther. 274: 458-68. Department of Pharmacology, Pharmacia Pharmaceuticals, Uppsala, Sweden. The experiments were done to investigate the presence and subtype of functionally presynaptic muscarinic receptors in cholinergic nerves of the guinea pig urinary bladder. Bladder strips were incubated with 3H-choline and superfused with Tyrode's solution containing eserine. Secreted 3H-acetylcholine was separated from 3H-choline. The electrically evoked 3H-acetylcholine secretion increased with the stimulation frequency. 3H-Acetylcholine secretion was enhanced by muscarinic antagonists, was depressed by carbachol and by alpha adrenoceptor agonists but was not influenced by drugs acting at beta adrenoceptors or purinoceptors. The rank order for the enhancing effect of muscarinic antagonist EC50 values was propantheline < atropine < methylatropine < N-desethyloxybutynin < UH-AH 37 < benzhexol < AQ-RA 741 < 4-DAMP < procyclidine < emepronium < secoverine < oxybutynin < tropicamide < promethazine < himbacine < hexahydrosiladifenidol < methoctramine = pirenzepine < dicyclomine < AF-DX 116, and the EC50 values correlated best with constants for the M4/m4 muscarinic receptor subtype. The enhancing effect of atropine was counteracted by carbachol; the effects of atropine and emepronium were not additive. The 3H-acetylcholine secretion was also enhanced by forskolin, 3-isobutyl-1-methylxanthine, 8-bromo cyclic AMP and dibutyryl cyclic AMP. The combined effects of atropine and forskolin were additive. These results suggest that the 3H-acetylcholine secretion in the guinea pig urinary bladder is regulated by a presynaptic muscarinic autoreceptor of the M4 subtype that is not coupled to adenylate cyclase.
    • Applebaum SM (1980). Pharmacologic agents in micturitional disorders. Urology. 16: 555-68.
    • Awad SA, Bryniak S, Downie JW and Bruce AW (1977). The treatment of the uninhibited bladder with dicyclomine. J Urol. 117: 161-3. Symptomatic treatment of the uninhibited bladder has presented a challenge because of the lack of an effective, well tolerated smooth muscle relaxant for the bladder that can be used during an extended interval. In a preliminary study oral dicyclomine produced resolution or significant improvement of symptoms in 24 of 27 patients and an increase in bladder capacity by an average of 137 plus or minus 26 ml. (91 plus or minus 22 per cent) after 8 weeks of therapy. Additional controlled trials definitely are warranted.
    • Awad SA, Wilson JW, Fenemore J and Kiruluta HG (1982). Dysfunction of the detrusor and urethra in multiple sclerosis: the role of drug therapy. Can J Surg. 25: 259-62. 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.
    • Beck RP, Arnusch D and King C (1976). Results in treating 210 patients with detrusor overactivity incontinence of urine. Am J Obstet Gynecol. 125: 593-6. Eighty (72.7 per cent) of 110 patients with detrusor overactivity (in controlled and uncontrolled series) showed improvement with parasympatholytic drug (propantheline bromide or dycyclomine HC1) therapy. Twenty per cent of patients on placebo therapy showed improvement. When standard surgery improved bladder neck funnelling, detrusor overactivity was improved in 77.3 per cent of cases. Surgery failed to improve detrusor overactivity in 54.5 per cent of patients who showed no significant bladder neck funnelling. Bladder neck funnelling appears to be a cause of detrusor overactivity in some women. Results with medical and surgical therapy were not associated with significant change in bladder capacity.
    • Downie JW and McGuire RP (1981). Antagonism of calcium-induced contraction in potassium-depolarized rabbit detrusor muscle strips by dicyclomine hydrochloride and rociverine. Can J Physiol Pharmacol. 59: 853-6. The musculotropic action of dicyclomine hydrochloride in bladder muscle has been attributed to its local anesthetic activity. In this study rabbit detrusor strips were depleted of calcium by incubation in Ca2+-free solution containing ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid (EGTA). Contractions elicited by replacement of Ca2+ during depolarization with 80 mM K+ were only slightly affected by atropine or scopolamine but were antagonized in a noncompetitive manner by dicyclomine and rociverine (pD2' = 4.89 and 4.61, respectively). These contractions were also blocked with greater potency by nifedipine (pD2' = 8.50) and with lesser potency by lidocaine (pD2' = 2.52). Procaine was ineffective up to 1 mM. Comparison of the antagonism produced by dicyclomine and rociverine with that produced by nifedipine or lidocaine did not help to define the mechanism of the musculotropic drugs. However, as rociverine is not a local anesthetic and procaine was not effective, it appears that the "local anesthetic" property is not sufficient to explain the action of these musculotropic drugs.
    • Downie JW, Twiddy DA and Awad SA (1977). Antimuscarinic and noncompetitive antagonist properties of dicyclomine hydrochloride in isolated human and rabbit bladder muscle. J Pharmacol Exp Ther. 201: 662-8. In isolated strips of bladder neck (prostatic capsule) and detrusor of rabbit and man, dicyclomine had minimal effect on the resting tension. Competitive antimuscarinic activity against carbachol could be demonstrated at doses of dicyclomine less than or equal to 1 X 10(-6) M, whereas at higher doses a noncompetitive action against both carbachol and potassium was observed. The ratio of dissociation constants relating to the noncompetitive and competitive actions, respectively, was about 1200, approximately 100 times higher than that previously reported in ileum. Dicyclomine was only about 1/30 as potent as atropine in competitive antimuscarinic activity. Dicyclomine hydrochloride may be useful in the clinical management of "uninhibited bladder."
    • Fischer CP, Diokno A and Lapides J (1978). The anticholinergic effects of dicyclomine hydrochloride in uninhibited neurogenic bladder dysfunction. J Urol. 120: 328-9. A preliminary study to assess objectively the effects of dicyclomine upon uncontrolled detrusor contractions and bladder capacity was undertaken in 14 patients with a cystometric diagnosis of uninhibited neurogenic bladder. Response was measured by cystometry performed 1, 2 and 4 hours after a 20 mg. oral dose. Of the 14 patients 11 had significant blockade of uninhibited contractions and a concomitant increase in bladder capacity. Similar but less dramatic changes were noted in the remaining 3 patients. Dicyclomine seems to have effective anticholinergic properties. No remarkable side effects were observed.
    • Khanna OP, DiGregorio GJ, Barbieri EJ, McMichael R and Ruch E (1979). In vitro study of antispasmodic effects of dicyclomine hydrochloride on vesicourethral smooth muscle of guinea pig and rabbit. Urology. 13: 457-62. Dicyclomine inhibition of acetylcholine-induced and barium chloride-induced isotonic contractions of the smooth muscle from three segments of the lower urinary tract (bladder body, bladder base, and proximal urethra) of the guinea pig and the rabbit was studied in vitro. In the guinea pig dicyclomine caused competitive inhibition of acetylcholine-induced contraction of the bladder body (1 x 10(-7) M to 1 x 10(-5) M) and the bladder base (1 x 10(-6) M, 1 X 10(-5) M) and was less potent than atropine and propantheline. In the rabbit significant blockade of acetylcholine-induced contractions occurred at dicyclomine concentrations of 5 x 10(-6) M to 3 x 10(-5) M in the bladder body and at 1 x 10(-5) M and 3 x 10(-5) M in the bladder base. In both species dicyclomine inhibitory effects were most marked in the bladder body, moderate in the bladder base, and minimal in the proximal urethra. Dicyclomine failed to cause inhibition of the barium chloride-induced contractions in the guinea pig vesicourethral smooth muscle. In rabbits, however, significant antagonism P less than 0.01) of barium chloride-induced muscle contraction was observed with dicyclomine at concentration 1 x 10(-5) M in both bladder body and the bladder base. The clinical implication of such properties of dicyclomine are discussed.
    • Levin RM and Wein AJ (1982). Direct measurement of the anticholinergic activity of a series of pharmacological compounds on the canine and rabbit urinary bladder. J Urol. 128: 396-8. Antimuscarinic therapy is used widely in the treatment of urine storage failure. Examples of antimuscarinic agents used clinically include atropine, propantheline bromide and glycopyrrolate. Other agents used in clinical urology that are believed to act at least in part by antimuscarinic activity include oxybutynin, imipramine and dicyclomine, These studies were designed to determine the relative potency of a variety of agents to compete directly for muscarinic cholinergic receptors isolated from the canine and rabbit urinary bladder. Radio-ligand binding assays for muscarinic receptors were performed with 10 nM 3H-QNB and various concentrations of the drugs under study. Of the agents tested, propantheline bromide, atropine, and glycopyrrolate were the potent muscarinic antagonists/unit of concentration. Oxybutynin and dicyclomine hydrochloride were 30 to 50 times less potent than atropine. Chlorpromazine and desmethylimipramine were approximately 500 times less potent than atropine. As expected, agents such as guanethidine, tranylcypramine and hexamethonium possessed little antimuscarinic activity.
    • Maggi CA and Meli A (1982). An in vivo procedure for estimating spasmolytic activity in the rat by measuring smooth muscle contractions to topically applied acetylcholine. J Pharmacol Methods. 8: 39-46. An in vivo procedure for evaluating potential organ selectivity of spasmolytics has been developed. This involves the determination of comparative potencies, expressed as DR10 of spasmolytics against contractions induced by topical application of acetylcholine on rat colon, rectum and urinary bladder. Experiments with two well known spasmolytics, namely N-butyl-scopolammonium bromide and dicyclomine HCl yielded results consistent with data reported in the literature. This procedure provides a rapid, inexpensive and rather accurate estimate of organ selectivity of spasmolytics.
    • Malone DC and Okano GJ (1999). Treatment of urge incontinence in Veterans Affairs medical centers. Clin Ther. 21: 867-77. Department of Pharmacy Practice, School of Pharmacy, University of Colorado Health Sciences Center, Denver 80262-0238, USA. Urinary incontinence has far-reaching medical, psychological, social, and economic effects. The objectives of this descriptive study were to examine utilization patterns and discontinuation rates of various pharmacologic agents used to treat symptoms of overactive bladder, primarily urge incontinence (UI), and to estimate the prevalence of urinary incontinence in the study population. Patient-level data regarding specific drugs used to treat UI and the use of diapers or pads over a 9-month period from October 1995 to May 1996 were retrospectively extracted from the medication databases of 9 Department of Veterans Affairs medical centers. A total of 2233 male patients were included in the analyses. Most patients were receiving oxybutynin chloride (39.8%), dicyclomine hydrochloride (16.0%), or imipramine hydrochloride (13.9%), and the remaining 30.3% were using flavoxate hydrochloride, propantheline bromide, hyoscyamine sulfate, and adult diapers or pads. Overall, 72.1% of patients had been prescribed daily dosages within the recommended dosing ranges for these medications. The majority (91.3%) of patients had not switched to another UI medication during the study period. Based on a chronic disease index, 47.6% of patients had 2 or fewer chronic diseases. Using pooled prevalence estimates, the estimated percentage of patients who had ever experienced UI in this population ranged from 7.4% to 20.8%; however, a considerably smaller percentage were taking medications for the treatment of UI. The results of this study suggest that oxybutynin, dicyclomine, and imipramine are the agents most commonly used to treat urinary incontinence within Veterans Affairs medical centers. The majority of patients who received a prescription for one of these drugs did not routinely refill the medication over the course of the study. There are many reasons for patients not to refill a prescription (eg, ineffectiveness, side effects, complications, obtaining the drug from another source), but the present study did not address the causes.
    • Monferini E, Giraldo E and Ladinsky H (1988). Characterization of the muscarinic receptor subtypes in the rat urinary bladder. Eur J Pharmacol. 147: 453-8. Department of Biochemistry, Istituto De Angeli S.p.A., Milan, Italy. We investigated the nature of the muscarinic receptors present in the rat urinary bladder by performing binding studies with various selective (pirenzepine, AF-DX 116, hexahydrosiladifenidol, benzhexol, 4-diphenyl-acetoxy-N-methyl piperidine methiodide, dicyclomine, secoverine) and classical (N-methylscopolamine, atropine) antagonists. Competition experiments were carried out against [3H]N-methyl scopolamine at 30 degrees C in Na+/Mg2+ HEPES buffer; non-specific binding was determined in the presence of 1 microM 3-quinuclidinyl benzilate. Of all the antagonists examined, only AF-DX 116 exhibited a heterogeneous binding profile (nH less than 1). Computer-assisted analysis showed that the data fitted best to a two-binding site model, revealing the existence of high and low affinity receptors. The affinity values of AF-DX 116, determined in binding experiments carried out in heart and gland homogenates, allowed us to classify the rat urinary bladder receptors into cardiac and glandular subtypes. We suggest that the glandular receptor subtype is involved in smooth muscle contraction, since AF-DX 116 was equally potent in inhibiting smooth muscle contraction and the secretion of saliva.
    • Nilvebrant L (1986). On the muscarinic receptors in the urinary bladder and the putative subclassification of muscarinic receptors. Acta Pharmacol Toxicol (Copenh). 59 Suppl 1: 1-45. The muscarinic cholinergic receptors in the urinary bladders of man, guinea pig, rat and rabbit were studied by means of a receptor binding technique, with l-quinuclidinyl [phenyl 4-3H]benzilate, (-)3H-QNB, as radioligand. The potential role of the receptors in the supersensitivity of the rat bladder to muscarinic agonists, following parasympathetic denervation, hypertrophy and urinary diversion, was also investigated. In addition, the binding of various unlabelled antimuscarinic drugs in the guinea pig bladder was compared to that in other tissues in order to study the putative muscarinic receptor subtypes, commonly referred to as M1 and M2. According to this classification the putative M1 receptors prevail in discrete areas of the brain, whereas the M2-receptors predominate in peripheral tissues, such as the exocrine glands and smooth muscles. The receptor density (but not the qualitative properties of the receptors) in the bladder differed between the species. The affinities of various antimuscarinic drugs were virtually identical in the guinea pig and human bladders. In both species, the binding data were found to correlate with functional in vitro data. In the rat bladder, the receptor density was increased after denervation but decreased, below control values, when the denervation was combined with urinary diversion. A decrease was also found after urinary diversion of innervated bladders, whereas the receptor density was unaffected by hypertrophy. These results suggest that the receptors are not involved in the development of supersensitivity and that the receptor levels may be influenced by the functional state of the bladder. Binding studies with classical muscarinic antagonists indicated that the receptors in the guinea pig bladder are indistinguishable from those in the ileum, heart, parotid gland and cerebral cortex. However, four drugs--namely, oxybutynin, dicyclomine, benzhexol and pirenzepine had a much higher affinity for the receptors in the parotid gland and cortex than for those in the other tissues. Moreover, dicyclomine and benzhexol, like pirenzepine, seemed in the cortex to distinguish between two classes of sites exhibiting high and low affinity. The high affinity sites could be selectively labelled with 3H-benzhexol. The ability of oxybutynin, dicyclomine, benzhexol and pirenzepine to discriminate between the receptors in the parotid gland and those in smooth muscle provides further evidence that the M1/M2 concept is inaccurate. The present data indicate that there may be three classes of muscarinic antagonist binding sites.
    • Nilvebrant L and Sparf B (1983). Differences between binding affinities of some antimuscarinic drugs in the parotid gland and those in the urinary bladder and ileum. Acta Pharmacol Toxicol (Copenh). 53: 304-13. Possible differences between the muscarinic receptors in the guinea pig urinary bladder and those in the ileum and the parotid gland were investigated, using a receptor binding technique. The affinities of 18 antimuscarinic drugs were indirectly derived from the ability to inhibit the receptor-specific binding of the radioligand (-)3H-QNB. The Hill coefficients were close to unity which indicated that the drugs were bound to apparently uniform populations of receptors within each tissue. In contrast to traditional muscarinic antagonists, four drugs - namely, oxybutynine, dicyclomine, benzhexol and pirenzepine - bound with a significantly higher affinity in the parotid gland than in the urinary bladder and ileum. A tendency towards reversed selectivity was found for secoverine. Thus, the present results further support the hypothesis that differences in muscarinic receptors between tissues exist, e.g. smooth muscle compared with parotid gland, which can be detected only by certain antimuscarinic drugs.
    • Nilvebrant L and Sparf B (1986). Dicyclomine, benzhexol and oxybutynine distinguish between subclasses of muscarinic binding sites. Eur J Pharmacol. 123: 133-43. The interactions of various unlabelled antimuscarinic drugs with the muscarinic receptors in the cerebral cortex, heart and urinary bladder were studied by a receptor binding technique, using (-)[3H]QNB as radioligand. In contrast to the other drugs examined, dicyclomine, benzhexol, oxybutynine and pirenzepine were bound with a significantly higher affinity in the cortex than in the heart and bladder. Furthermore, not only pirenzepine, but also dicyclomine and benzhexol were capable of distinguishing between two populations of muscarinic binding sites in the cortex. The low affinity sites for these drugs in the cortex were characterised by dissociation constants which were similar to those determined in the heart and the bladder, respectively. It was concluded that dicyclomine and benzhexol, like pirenzepine, are selective antagonists at the putative M1-receptor. Oxybutynine exhibited the same affinity profile but the tissue selectivity of this drug was less pronounced.
    • Noronha-Blob L, Lowe VC, Hanson RC and U'Prichard DC (1987). Heterogeneity of muscarinic receptors coupled to phosphoinositide breakdown in guinea pig brain and peripheral tissues. Life Sci. 41: 967-75. Muscarinic receptors coupled to phosphoinositide hydrolysis (PI) are present in guinea pig bladder and colon. Compared to rat cerebral cortex, an extensively studied muscarinic/PI turnover system, all agonists were more potent and efficacious in both bladder and colon. The "M1-selective antagonists", pirenzepine and dicyclomine, were much more potent (Ki = 1-5 nM) and selective (300 to 500-fold) at both rat and guinea pig brain and guinea pig colon receptors, compared to PI-coupled receptors in guinea pig bladder. In contrast, "M2-selective antagonists", AF-DX 116 and HHSiD, were 2-6 fold more potent in bladder than in brain, while HHSiD was very potent in the colon (50 times more potent than in brain). These results suggest a pharmacological heterogeneity of PI-linked muscarinic receptors. If muscarinic receptors with a low affinity for pirenzepine are defined as M2, these results show that the guinea pig bladder contains PI-linked M2 muscarinic receptors, whereas the guinea pig colon contains PI-linked M1 receptors.
    • Peterson JS, Patton AJ and Noronha-Blob L (1990). Mini-pig urinary bladder function: comparisons of in vitro anticholinergic responses and in vivo cystometry with drugs indicated for urinary incontinence. J Auton Pharmacol. 10: 65-73. Nova Pharmaceutical Corporation, Baltimore, Maryland 21224-2788. 1. Studies of carbachol-induced contractions on mini-pig bladder tissue strips in vitro demonstrated that antagonist drugs produced a rank order of potency similar to that observed in guinea-pig tissues: propantheline approximately atropine greater than oxybutynin greater than dicyclomine greater than HHSiD greater than imipramine greater than terodiline approximately AF-DX 116. The drugs appeared to show competitive antagonism and the tissues exhibited resistance to complete cholinergic blockade. 2. Cytometry performed in vivo on awake mini-pigs also showed that i.v. cholinergic antagonists produced a dose-dependent depression of peak intravesical bladder pressure (PvesP) during slow filling of the bladder using urethral catheters, with a rank order of potency: atropine greater than oxybutynin approximately propantheline greater than HHSiD approximately dicyclomine greater than terodiline. Other parameters of the cystometrogram were unaffected by the antagonists, except for residual volume, which generally increased after drug treatment. 3. Hexahydrosiladifenidol (HHSiD), an ileal-selective competitive muscarinic antagonist, was about as effective an antagonist as the clinically useful drugs oxybutynin or dicyclomine, both in vitro and in vivo, suggesting that HHSiD may have useful therapeutic effects for the treatment of urinary incontinence. 4. Correlation of the rank order of potency for muscarinic antagonism between mini-pigs and guinea-pigs was very high in vitro (r = 0.97, P less than 0.05), as was the correlation among the drugs for their ability to depress PvesP of the cystometrogram in vivo (r = 0.89, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS).
    • Seruca H (1989). Vesicoureteral reflux and voiding dysfunction: a prospective study. J Urol. 142: 494-8; discussion 501. Department of Pediatrics, Hospital de Santa Maria, Universidade Classica de Lisboa, Lisbon, Portugal. We prospectively studied 53 young children (45 less than 4 years old) between 1985 and 1988 with primary vesicoureteral reflux (grades I to V, 74 ureters). All patients had elevated bladder pressures during bladder filling and/or voiding on urodynamic evaluation, which sometimes were associated with abnormal perineal muscle activity. Baclofen, flavoxate, dicyclomine and diazepam were given individually or in combination for each type of dysfunction for 12 to 30 months. Reflux disappeared in 68 ureters (91.8 per cent) and it was downgraded in 6 (8.2 per cent). Urodynamic evaluation at the end of treatment revealed normal bladder pressures in 46 children (83.7 per cent of the ureters in which reflux resolved). Another group of 48 children with primary vesicoureteral reflux (grades I to IV, 67 ureters) seen between 1980 and 1985 was reviewed retrospectively. All patients had been treated with prophylactic antibiotics only. Reflux resolved in 53.7 per cent of the ureters, and it was downgraded in 19.4 per cent, unchanged in 22.4 per cent and upgraded in 4.5 per cent. Urodynamic studies performed in 1985 showed that all persistent cases of reflux in the retrospective group had urodynamic findings similar to those found in the prospective group. These data suggest that vesicoperineal incoordination as well as bladder instability can be important factors in causing and perpetuating reflux, and that medical treatment of these factors individually or in combination may affect therapeutic perspectives of this pathological condition.
    • Soulard C, Pascaud X, Roman FJ, Grouhel A and Junien JL (1992). Pharmacological evaluation of JO 1870: relation to the potential treatment of urinary bladder incontinence. J Pharmacol Exp Ther. 260: 1152-8. Institut de Recherche Jouveinal, Fresnes, France. The effect of p.o. administered JO 1870 [(-)-1-(p-chlorophenyl)-N,N- dimethyl-1-ethyl(4-phenyl)-but-3-en-1-ylamine, hydrochloride] on the urinary bladder cystometrogram has been investigated in the unanesthetized rat. The effects of JO 1870 have been compared with those of morphine and reference drugs currently used for the treatment of urinary incontinence in humans. JO 1870 (2.5-25 mg/kg) dose-dependently increased the bladder capacity and the threshold pressure responsible for urination. These effects were antagonized by the i.v. administration of naloxone (0.2 mg/kg). In comparison, morphine (2.5-25 mg/kg) moderately increased urinary volume and threshold pressure. Different anticholinergic drugs (propantheline bromide, 10 mg/kg; terodiline, 25 mg/kg; dicyclomine, 25 mg/kg) had no significant effects on either parameter and the antidepressant clomipramine (25 mg/kg) decreased both. In vitro, JO 1870 specifically displaced [3H]-[D-Ala2,MePhe4,Gly5-(ol)]enkephalin from binding sites in guinea pig whole-brain membranes and rat thalamus; the sodium shift ratio obtained from [3H]naloxone binding was 16. These results suggest that JO 1870 has some opioid agonist activity. JO 1870 (2.5-300 mg/kg) had few effects on cardiorespiratory, gastrointestinal or nociceptive systems in rats. Together, these results indicate that JO 1870 is a nonanticholinergic agent that potently increases bladder capacity, likely through an opioid mechanism, and may have potential use in the treatment of urinary incontinence.
    • Thompson IM and Lauvetz R (1976). Oxybutynin in bladder spasm, neurogenic bladder, and enuresis. Urology. 8: 452-4. 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.

  8. #8
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    After reading the abstracts the majority referenced the bladder. I use a condom catheter and void spontaneously or by taping and crede.

    Is this going cause AD or urine retention?

    It is suposed to be for bowel spasms

  9. #9
    Super Moderator Sue Pendleton's Avatar
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    Originally posted by Cris:

    After reading the abstracts the majority referenced the bladder. I use a condom catheter and void spontaneously or by taping and crede.

    Is this going cause AD or urine retention?

    It is suposed to be for bowel spasms
    Cris, if it is very close to Levsin I can tap if my bladder is full and even though I also take Ditropan XL I can go some. I don't tap much because I have to be on the toilet (female, ya know) and my bladder is kind of touchy about it. Like it will feel spazey and a bit painful after I void by tapping. I tend to do this if I have a borderline UTI to try and flush the bugs. Levsin also comes in a fast acting sublingual form. If your med does you might try it that way first. Then if you can't void it will wear off quickly and you should be ok.

    If your IBS is diarrhea dominant there are other drugs to help control it if the dicyclomine doesn't work out for you.

    Courage doesn't always roar. Sometimes courage is the quiet voice at the end of the day saying, "I will try again tomorrow."

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