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 case of carcinosarcoma of the urinary bladder is reported. Transurethral resection was performed. Histologically the tumorous mass was composed of osteosarcoma, squamous cell carcinoma and transitional cell carcinoma. The histological findings, immunohistochemical features and clinical manifestations of bladder carcinosarcoma are discussed in relation to the literature.
Intracerebroventricular morphine consistently inhibited spontaneous urinary bladder contractions recorded from the anesthetized rat. This effect was reversed by naloxone and appeared to be exerted within the forebrain. Neither dynorphin-(1-13) nor U-50, 488 (kappa-agonists) affected bladder motility. Ethylketocyclazocine inhibited contractions only at higher doses, possibly due to mu-receptor interactions. Bladder activity was consistently inhibited by the mu-agonists morphiceptin and [D-Ala2, MePhe4, Gly-(ol)5]enkephalin (DAGO) and by [D-Ala2, D-Leu5]enkephalin (DADLE, delta-agonist). DAGO was the most potent compound tested. These observations support the involvement of mu- and possibly delta-receptors in the centrally mediated inhibition of urinary bladder motility by opioids.
AIMS: Several pathophysiological conditions in the urinary bladder, for example, ischemia/reperfusion and inflammation are characterized by the formation of reactive oxygen species (ROS). The ROS are highly toxic because they can destroy proteins, DNA, and lipids. The aim of this study was to investigate the effect of oxidative stress on excitation-contraction coupling of detrusor smooth muscle. MATERIALS AND METHODS: Smooth muscle strips were dissected from pig urinary bladder and mounted in organ baths. Oxidative stress was mimicked by the addition of Cumene hydroperoxide (CHP), a lipophilic hydroperoxide, to the organ baths. Contractile responses to electrical field stimulation (EFS: 4-32 Hz), carbachol (10(-8)-3 x 10(-5) M), potassium (65.3 mM), and ATP (1 mM) were monitored before and after the addition of CHP. RESULTS: Responses of detrusor strips to EFS were for the greater part based on neurogenic stimulation and the release of acetylcholine. CHP diminished contractile responses to EFS and carbachol to the same extent. The pD(2) value of the carbachol concentration-response curve decreased significantly after exposure to 0.1 mM, 0.4 mM, 0.8 mM CHP. Furthermore the maximal effect obtained with carbachol was significantly reduced after 0.1 mM, 0.4 mM, and 0.8 mM CHP treatment. Contractions induced by potassium and ATP were significantly less affected by oxidative stress compared to EFS- and carbachol-induced responses of comparable amplitude. CONCLUSIONS: The results of our study demonstrate that oxidative stress induced by CHP affects pig bladder contractility. The muscarinic receptor signaling system is severely damaged. L-type calcium channels and the contractile system are less affected and cholinergic nerves remain largely unaffected.
Dietary supplementation with bisacodyl at concentrations ranging from 1 to 0.3% was found to induce both calculi and epithelial proliferative lesions, including a transitional-cell carcinoma, in the urinary bladder of F344/DuCrj rats. In order to clarify the relationship between the bisacodyl-associated urinary bladder calculi and the development of proliferative lesions in the urinary bladder, male and female rats were administered bisacodyl-diets at concentrations of 0.3, 0.1, and 0.03% for 32 wk. Both sexes of animals treated with bisacodyl suffered from diarrhea throughout the experimental period. Epithelial proliferative lesions and calculus formation were observed only in the urinary bladder of male rats given the 0.3% bisacodyl diet. Proliferative lesions and increases of bromouracil deoxyriboside (BUdR) labeling indices were found only in the urinary bladder epithelium of rats with calculi, the severity of the former correlating with the calculus weight and being most marked in the dome areas, which are susceptible to physical stimulation. These findings indicate a close relationship between the development of proliferative lesions and the existence of calculi in the urinary bladder, and suggest that bisacodyl-induced proliferative lesions are not caused directly by bisacodyl per se but are secondary to calculus formation.
Paired toad urinary hemibladders were incubated with [35S]methionine in the presence (experimental) or absence (control) of aldosterone. Short-circuit current was used to monitor aldosterone-induced Na+ transport. Protein synthesis in epithelial cell subcellular fractions (cytosolic, microsomal, mitochondrial) was evaluated by gradient polyacrylamide gel electrophoresis and autoradiography. Aldosterone-induced proteins were identified in the cytosolic and microsomal fractions (70 000 and 15 000 daltons, respectively). These results represent the first demonstration of aldosterone-induced proteins in subcellular fractions of epithelial cells derived from single toad urinary hemibladders.
The urinary and urothelial effects of the frequent handling necessary for obtaining fresh-voided urine specimens were evaluated in 5-wk-old male F-344 rats fed control diet or diet containing 7.5% sodium saccharin. Frequent handling consisted of holding rats by the back of the neck in a position to obtain fresh-voided urine directly into centrifuge tubes 3 times per week for 10 weeks, whereas seldomly handled control rats received this treatment only twice during the entire 10 weeks. The urothelium of frequently handled rats fed control diet showed superficial necrosis and regenerative hyperplasia as observed by light and scanning electron microscopy. These changes were not observed in rats fed control diet that were seldomly handled. The necrosis and hyperplasia were not as pronounced in frequently handled rats fed control diet as in seldomly handled, sodium-saccharin-treated rats, but handling also potentiated the severity of the changes produced by sodium saccharin feeding. The urothelial exfoliation and consequent regenerative hyperplasia are likely secondary effects of stress.
Instillation of cold water into the urinary bladder has been used as a diagnostic test to evaluate neurogenic dysfunctions of the lower urinary tract (LUT). This study examined the effects of cold stimulation on the LUT of urethan-anesthetized rats. Urinary bladder pressure and external urethral sphincter (EUS) electromyogram (EMG) were recorded during cystometrograms in which body- or room-temperature saline was infused continuously into the bladder and voided through the urethra. Subsequent infusion of cold saline (6-8 degrees C) into the bladder increased by approximately 100% the duration and amplitude of supraspinal reflex bladder contractions, increased baseline bladder pressure, increased the pressure threshold for inducing micturition, and increased EUS EMG activity. Blocking EUS activity by transecting the pudendal nerves or by administering a neuromuscular blocking agent markedly reduced or eliminated the effect of cold stimulation. Capsaicin pretreatment suppressed the effect of cold stimulation. It is concluded that cold temperatures stimulate capsaicin-sensitive C fiber bladder afferents that reflexly activate the EUS, producing detrusor and sphincter dyssynergia and increasing urethral outlet resistance. This in turn increases the amplitude and duration of bladder contractions during voiding.
OBJECTIVES: Oat cell carcinoma of the urinary bladder is extremely uncommon. To date, 87 cases have been reported in the literature. Histologically, these tumors are similar to oat cell carcinoma of the lung and in slightly more than half of the cases the tumor is associated with another carcinomatous component: urothelial, squamous carcinoma, adenocarcinoma or, more rarely, sarcomatoid carcinoma. A case of sarcomatoid small cell carcinoma is described herein. METHODS/RESULTS: We report a case of sarcomatoid small cell carcinoma of the urinary bladder in a 79-year-old female patient. The tumor was in the advanced stages and was unamenable to resection. The patient was treated with multi-drug systemic chemotherapy, but she died five months after diagnosis. Light microscopy disclosed a carcinomatous component similar to oat cell carcinoma of the lung that stained with epithelial and neuroendocrine markers. The sarcomatoid component was histologically nondescript and showed extensive immunoreactivity to mesenchymal and epithelial markers. CONCLUSIONS: Sarcomatoid small cell carcinoma of the bladder is rare. To our knowledge, only five cases have been previously reported. It is aggressive, metastasizes early and has a poor diagnosis. Surgical resection with adjuvant multidrug systemic chemotherapy is currently the best available treatment.
1. A total of sixty-five sacral afferent neurones with myelinated fibres supplying the urinary bladder was recorded from the sacral roots S2 in anaesthetized cats. All afferent units were identified with electrical stimulation of the pelvic nerve. The discharge properties were quantitatively evaluated using slow filling at rates of 1-2 ml min-1 and isotonic distension to preset pressure levels. Eight afferents were studied prior to and after acute sacral de-efferentation of the urinary bladder. 2. All afferent units were silent when the bladder was empty and responded in a graded manner to an increase of intravesical pressure. During slow filling the level of afferent activity correlated closely with the level of the intravesical pressure. All afferents behaved like slowly adapting mechanoreceptors with both a dynamic and static component of their discharge. With the exception of two units the intraluminal pressure threshold was below 25 mmHg. Thus virtually all myelinated afferents respond in the pressure range that is reached during a non-painful micturition cycle. 3. The stimulus-response functions of the afferents were similar regardless of whether intravesical pressure was increased by slow filling or by distension. However, during slow filling stimulation response functions often exhibited steeper slopes between 5 and 25 mmHg indicating that relatively small changes of intravesical pressure result in large changes of afferent activity. Nevertheless, all units displayed monotonically increasing stimulus response functions throughout the innocuous and noxious pressure level. 4. The stimulus-response functions of the afferent neurones did not change after acute de-efferentation of the urinary bladder, although the rapid phasic fluctuations of afferent activity that are produced by small contractions of the urinary bladder under normal conditions largely disappeared. This means that contractions and distension activate the afferent endings by a common mechanism. 5. It is concluded that the myelinated sacral afferents of the urinary bladder form a homogeneous population which encodes all information necessary for the normal regulation of this organ. Furthermore, this set of afferents mediates all sensations which may reach consciousness within a normal micturition cycle.
Urinary bladder absorption of stable and radiofluoride was studied as a function of pH in anesthetized rats to further evaluate the influence of pH gradients on fluoride transport. Buffered pH values and stable fluoride concentrations ranged from 1.85 to 7.90 and from 0.012 to 8.81 mM, respectively. [14c]inulin served as a marker for solute concentration changes due to water migration or dilution. The results indicate that bladder fluoride absorption is inversely related to pH over the 1.85-5.50 range. Mean, 15-min radiofluoride absorption values of 70% at pH 1,85, 37% at pH 3.95, and 5% at pH 5.50 WERE OBSERVED. These fractional absorption values were not significantly influenced by carrier fluoride concentration, the buffers used, or the presence of urine. Above pH 5.50, pH-independent absorption occurs to a slight extent. The results are consistent with a first-order absorptive process which occurs by the nonionic diffusion of hydrogen fluoride.
In this article, the role of MR imaging in the management of carcinoma of the urinary bladder is reviewed and illustrated. The appearance of the normal urinary bladder and of bladder carcinoma on MR images is shown. Important factors for optimal MR imaging of urinary bladder carcinoma are reviewed. New developments such as three-dimensional and fast spin-echo sequences and the use of contrast agents, endorectal imaging, and phased array coils are discussed. Finally, the value of MR imaging in the staging of bladder carcinoma is described, and MR staging is compared with clinical staging, staging based on findings from intravesical sonography, and CT staging.
Nephrogenic metaplasia of urinary bladder, with synonyms of nephrogenic adenoma, mesonephric adenoma or adenomatoid tumour is a rare metaplastic lesion which can be clinically as well as morphologically mistaken for malignancy of the bladder. We present one case because of its rarity and also to emphasize the need for increase in its awareness both among urologists and pathologists, leading to accurate identification of the lesion.
A case report of a chordoid sarcoma of the urinary bladder of an 81 years old man is presented. After the first description of the extraskeletal chordoid sarcoma in 1948, this is the first report of the tumor of the urinary bladder.
Benign urinary bladder tumors are very rare, leiomyoma being the most common among them. We wish to report a case and discuss the radiological findings with special emphasis on magnetic resonance (MR) imaging.
OBJECTIVE: To evaluate the effect of intravesical resiniferatoxin on spinal c-fos expression and bladder volume at reflex micturition in rats with chronic urinary bladder inflammation. MATERIALS AND METHODS: Of three groups of female Wistar rats, group 1 received cyclophosphamide (75 mg/kg body weight) intraperitoneally every third day (cyclophosphamide is an antitumoral agent that induces bladder inflammation after urinary excretion of its metabolite, acrolein); group 2 comprised sham-inflamed rats that received saline instead of cyclophosphamide, and group 3 received cyclophosphamide, as group 1, every third day but plus 10 nmol/L resiniferatoxin intravesically, through a urethral catheter, at 7 days. At 8 days, under urethane anaesthesia, a needle was inserted in the bladder dome and saline infused at 6 mL/h for 2 h. Finally the animals were perfusion-fixed through the ascending aorta with 4% paraformaldehyde. Transverse sections cut from L6 spinal cord segments were immunoreacted for Fos protein and positive cells in the dorsal horn counted. In a further set of equal groups the bladders were prepared in the same way under urethane anaesthesia and after 30-min of stabilization, saline was infused at 6 mL/h and the volume evoking reflex micturition determined. RESULTS: The mean (SD) number of positive c-fos cells per spinal cord section was 85 (21), 42 (9) (P = 0.002) and 55 (10) in groups 1 to 3, respectively; the values for group 2 and 3 were similar (P = 0.22) and statistically less than that of group 1 (P = 0.02). Reflex micturition occurred at, respectively, 0.26 (0.09), 0.49 (0.18) and 0.52 (0.11) mL, being similar in group 2 and 3 (P = 0.74) but lower in group 1 (P = 0.003). CONCLUSION: Intravesical resiniferatoxin decreases c-fos expression and increases bladder capacity in chronically inflamed rat bladders. These findings suggest that desensitizing the vanilloid receptor type 1 by intravesical resiniferatoxin is relevant to the treatment of pain and voiding frequency in patients with chronic inflammatory bladder conditions.
Effects of X-irradiating the urinary bladder of female F344 rats with a single dose of 20 Gy were studied by light and electron microscopy. The animals were killed 1 week-20 months post-irradiation, and all tissues of the bladder wall were found to be affected by the irradiation. In the urothelium, damage was initially restricted to the basal cells but slowly extended to intermediate cells, and by 6 months post-irradiation the urothelium was focally hyperplastic. Twenty months post-irradiation, transitional-cell carcinomas were found in 10 of the surviving 17 animals (59%). The blood vessels in the bladder wall showed damage to both the endothelial cells and the smooth muscle. The fibroblasts in the connective tissue of the bladder wall appeared to show increased secretion after irradiation, and there was abundant collagen deposition, resulting in severe fibrosis of the bladder wall. After a latent period of a few months, focal degeneration and extensive necrosis of the smooth muscle cells were seen, leading to severe destruction and disorganization of the muscular coats of the bladder wall. Thus, a single dose of irradiation of 20 Gy was sufficient to produce severe fibrosis of the bladder wall with smooth muscle degeneration and to induce carcinoma of the urothelium in most of the treated animals within 20 months.
The effect of peptide vilon (Lys-Glu) on urinary bladder carcinogenesis in rats was studied. Urinary bladder tumors were induced with a selective carcinogen N-butyl-N-(4-hydroxybutyl)nitrosamine. The tumors developed in 56% vilon-treated animals and in 75.5% controls. Vilon 2-fold decreased the incidence of preneoplastic and early neoplastic changes in urinary bladder mucosa and significantly inhibited carcinogenesis.
AIMS: Obstruction of the urinary bladder outlet induces detrusor smooth muscle (DSM) hypertrophy. The goal of this study was to determine whether the composition of thin filament-associated proteins, known to play important roles in cytoskeletal structure and/or the regulation of contraction, is altered in DSM during hypertrophy. METHODS: DSM hypertrophy was induced in male rabbits by partial ligation of the urethra. Sham-operated rabbits served as a control. Reverse transcriptase-polymerase chain reaction (RT-PCR) and real-time PCR revealed a significant increase in the expression of mRNAs for basic (h1) calponin (CaP), and alpha-isoform of tropomyosin (Tm) in hypertrophied DSM compared to controls. Western blotting and two-dimensional (2-D) gel electrophoresis showed enhanced expression of these proteins and also a significant increase in the expression of beta-non muscle and gamma-smooth muscle actin in the DSM from obstructed bladders, while alpha-actin remained constant. RESULTS: Enhanced expression of these proteins in the DSM from obstructed bladders was confirmed by immunofluorescence microscopy. Double immunostaining with Cap/Tm and alpha/beta-actin-specific antibodies showed co-localization of these proteins in myocytes. Colocalization of smooth muscle specific myosin and CaP to cytoplasmic filaments in cells dissociated from the hypertrophied DSM indicated that these cells are differentiated smooth muscle cells. CONCLUSIONS: The change in the isoforms of actin, Cap, and Tm may be part of the molecular mechanism for bladder compensation in increased urethral resistance.