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Bladder Weight (bladder + weight)
Selected AbstractsEffects of chronic treatment with vardenafil, a phosphodiesterase 5 inhibitor, on female rat bladder in a partial bladder outlet obstruction modelBJU INTERNATIONAL, Issue 7 2009Seiji Matsumoto OBJECTIVES To investigate whether vardenafil, a phosphodiesterase 5 (PDE-5) inhibitor, would protect the bladder from decompensatory changes in a 4-week rat bladder outlet obstruction (BOO) model, as evidence has been accumulating that PDE-5 inhibitors improve lower urinary tract symptoms (LUTS) in patients with benign prostatic hyperplasia (BPH). MATERIALS AND METHODS In all, 50 12-week-old female Sprague-Dawley rats were divided into five equal groups; group 1, sham operated vehicle control rats; group 2, BOO vehicle rats; group 3,5, BOO rats given oral vardenafil at 5, 20, 80 mg/L, respectively. Vardenafil was given in drinking water from the day of surgery. At 4-weeks after the introduction of BOO, vardenafil was washed-out by giving water for 24,48 h, and then the bladder was excised and dissected into four longitudinal strips for isometric organ-bath assay. Contractile responses of bladder strips to electrical field stimulation (EFS), carbachol and KCl was determined for each group. RESULTS BOO induced a significant increase in bladder weight in group 2 compared with group 1. Bladder weights of groups 3,5 were not significantly different from that of group 2. The contractile forces in response to EFS, carbachol and KCl in group 2 were 30.7,51.7% of those in group 1. Vardenafil treatment in groups 3,5 generally did not block the BOO-induced reduction of contractile force in the bladder strips. However, treatment with a high dose of vardenafil resulted in a significant increase in the contractile response to carbachol (78.4% group 5 vs 51.7% group 2). CONCLUSION Chronic treatment with a high dose of vardenafil protected the rat bladder from BOO-induced contractile dysfunction to carbachol. [source] External urethral sphincter activity in diabetic ratsNEUROUROLOGY AND URODYNAMICS, Issue 5 2008Guiming Liu Abstract Aim To examine the temporal effects of diabetes on the bladder and the external urethral sphincter (EUS) activity in rats. Methods Female Sprague-Dawley rats (n,=,24) were divided into two groups: streptozotocin-induced diabetic rats and age-matched controls. Cystometrograms (CMGs) were taken under urethane anesthesia and electromyograms (EMG) of the EUS were evaluated in all rats at 6 and 20 weeks after diabetes induction. After EMG assessment, the tissues of the urethra were harvested for morphological examination. Results Diabetes caused reduction of body weight, but an increase in bladder weight. CMG measurements showed diabetes increased threshold volume, contraction duration, high-frequency oscillations (HFO), and residual volume. Peak contraction amplitude increased in 6-week but not 20-week diabetic rats. EUS-EMG measurements showed increased frequency of EUS-EMG bursting discharge during voiding in 6-week diabetic rats (8.1,±,0.2 vs. 6.9,±,0.6/sec) but not in 20-week (5.8,±,0.3 vs. 6.0,±,0.2/sec) diabetic rats compared with controls. EUS-EMG bursting periods were also increased in both 6-week and 20-week diabetic rats compared with controls. EUS-EMG silent periods were reduced in 6-week diabetic rats, but were not changed in 20-week diabetic rats compared with controls. Active periods did not change in 20-week diabetic rats, but increased in 6-week diabetic rats compared with controls. Morphometric analysis showed atrophy of the EUS after 20 week but not 6 weeks of DM induction. Conclusions Our data indicates diabetes causes functional and anatomical abnormalities of the EUS. These abnormalities may contribute to the time-dependent bladder dysfunction in diabetic rats. Neurourol. Urodynam. 27:429,434, 2008. © 2008 Wiley-Liss, Inc. [source] The effect of tamsulosin on the response of the rabbit bladder to partial outlet obstructionNEUROUROLOGY AND URODYNAMICS, Issue 1 2006Robert M. Levin Abstract Aim To determine if tamsulosin treatment prevents or decreases the incidence and severity of outlet obstruction-induced bladder dysfunction in rabbits. Materials and Methods Male New Zealand White rabbits were treated with tamsulosin or vehicle for 4 weeks with treatments initiated 1 week prior to sham or obstruction surgery. Cystometry was done on anesthetized rabbits 21 days after surgery. The bladders were then removed, weighed, and prepared for in vitro whole bladder studies. Responses to 32 Hz field stimulation (FS), carbachol, phenylephrine, and KCl were measured. Results Obstruction resulted in a significant increase in bladder weight, which was unchanged by tamsulosin treatment and a significant increase in micturition pressure in the vehicle-treated group but not in the tamsulosin-treated group. Compliance was significantly decreased in both obstructed groups. The vehicle-treated obstructed rabbits had a very sharp increase in intravesical pressure as the bladder reached capacity; this was not seen in the tamsulosin-treated obstructed rabbits. Tamsulosin did not change the pattern of modifications in contractile responses induced by bladder outlet obstruction. Conclusions In vitro responses of vehicle and tamsulosin-treated obstructed rabbit groups in this study were similar. A greater micturition pressure was found for the vehicle-treated obstructed group than for the tamsulosin-treated obstructed group, which was probably due to decreased urethral resistance in the latter. On a functional basis, the higher compliance at capacity and decreased micturition pressure in the tamsulosin-treated obstructed group would be considered beneficial for bladder function. Neurourol. Urodynam. © 2005 Wiley-Liss, Inc. [source] Urodynamic evaluation of fesoterodine metabolite, doxazosin and their combination in a rat model of partial urethral obstructionBJU INTERNATIONAL, Issue 2 2010Claudius Füllhase OBJECTIVE To evaluate the urodynamic effects of fesoterodine, a new antimuscarinic agent, alone and combined with doxazosin, in a rat model of partial urethral obstruction (PUO), as 35,83% of men with bladder outlet obstruction (BOO) secondary to benign prostatic hyperplasia (BPH) have overactive bladder (OAB) syndrome, and as the combination of ,1 -adrenoceptor- and muscarinic-receptor antagonists has been proposed to be beneficial for these patients. MATERIALS AND METHODS Thirty-seven male Sprague-Dawley rats (250 g) had surgically induced PUO; 2 weeks later they were evaluated by cystometry with no anaesthesia or any restraint. After a 1-h period either 5-hydroxymethyl tolterodine (5-HMT, the active metabolite of fesoterodine, previously known as SPM 7605), doxazosin or a combination of both, was given intravenously (0.1 mg/kg body weight), and cystometry was continued for another 45 min. Fifteen healthy, age-matched rats served as a control. RESULTS At 2 weeks after surgery the obstructed rats had an greater bladder weight, threshold pressure (TP) and micturition frequency (MF), and lower bladder capacity (BCap) and micturition volume (MV) than the controls. 5-HMT did not cause urinary retention in obstructed rats, but decreased TP, maximum pressure (MP), spontaneous bladder activity (SA) and, paradoxically, increased MF. Doxazosin alone decreased TP, MP, MF and increased BCap and MV. 5-HMT and doxazosin together did not depress the ability to empty the bladder, and showed decreased TP, MP and SA. CONCLUSIONS 5-HMT, alone and in combination, did not impair the voiding ability in obstructed rats. Doxazosin counteracted some of the ,negative' effects of 5-HMT in this model (increase of MF) and did not attenuate the ,positive' effects (decrease of bladder SA). In this model, the combination of 5-HMT and doxazosin appeared to be urodynamically safe and well tolerated. [source] Effects of chronic treatment with vardenafil, a phosphodiesterase 5 inhibitor, on female rat bladder in a partial bladder outlet obstruction modelBJU INTERNATIONAL, Issue 7 2009Seiji Matsumoto OBJECTIVES To investigate whether vardenafil, a phosphodiesterase 5 (PDE-5) inhibitor, would protect the bladder from decompensatory changes in a 4-week rat bladder outlet obstruction (BOO) model, as evidence has been accumulating that PDE-5 inhibitors improve lower urinary tract symptoms (LUTS) in patients with benign prostatic hyperplasia (BPH). MATERIALS AND METHODS In all, 50 12-week-old female Sprague-Dawley rats were divided into five equal groups; group 1, sham operated vehicle control rats; group 2, BOO vehicle rats; group 3,5, BOO rats given oral vardenafil at 5, 20, 80 mg/L, respectively. Vardenafil was given in drinking water from the day of surgery. At 4-weeks after the introduction of BOO, vardenafil was washed-out by giving water for 24,48 h, and then the bladder was excised and dissected into four longitudinal strips for isometric organ-bath assay. Contractile responses of bladder strips to electrical field stimulation (EFS), carbachol and KCl was determined for each group. RESULTS BOO induced a significant increase in bladder weight in group 2 compared with group 1. Bladder weights of groups 3,5 were not significantly different from that of group 2. The contractile forces in response to EFS, carbachol and KCl in group 2 were 30.7,51.7% of those in group 1. Vardenafil treatment in groups 3,5 generally did not block the BOO-induced reduction of contractile force in the bladder strips. However, treatment with a high dose of vardenafil resulted in a significant increase in the contractile response to carbachol (78.4% group 5 vs 51.7% group 2). CONCLUSION Chronic treatment with a high dose of vardenafil protected the rat bladder from BOO-induced contractile dysfunction to carbachol. [source] Pharmacokinetics, dose-range, and mutagenicity studies of methylphenidate hydrochloride in B6C3F1 mice,,ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 8 2008Mugimane G. Manjanatha Abstract Methylphenidate hydrochloride (MPH) is one of the most frequently prescribed pediatric drugs for the treatment of attention deficit hyperactivity disorder. In a recent study, increased hepatic adenomas were observed in B6C3F1 mice treated with MPH in their diet. To evaluate the reactive metabolite, ritalinic acid (RA) of MPH and its mode of action in mice, we conducted extensive investigations on the pharmacokinetics (PK) and genotoxicity of the drug in B6C3F1 mice. For the PK study, male B6C3F1 mice were gavaged once with 3 mg/kg body weight (BW) of MPH and groups of mice were sacrificed at various time points (0.25,24 hr) for serum analysis of MPH and RA concentrations. Groups of male B6C3F1 mice were fed diets containing 0, 250, 500, 1,000, 2,000, or 4,000 ppm of MPH for 28 days to determine the appropriate doses for 24-week transgenic mutation studies. Also, the micronucleus frequencies (MN-RETs and MN-NCEs), and the lymphocyte Hprt mutants were determined in peripheral blood and splenic lymphocytes, respectively. Mice fed 4,000 ppm of MPH lost significant BW compared to control mice (P < 0.01). There was a significant increase in the average liver weights whereas kidneys, seminal vesicle, testes, thymus, and urinary bladder weights of mice fed higher doses of MPH were significantly lower than the control group (P , 0.05). There was no significant increase in either the Hprt mutant frequency or the micronucleus frequency in the treated animals. These results indicated that although MPH induced liver hypertrophy in mice, no genotoxicity was observed. Environ. Mol. Mutagen., 2008. Published 2008 Wiley-Liss, Inc. [source] | ||||||||||