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We report on a rare in utero appearance of urinary bladder perforation, urinary ascites, and bilateral contained urinomas secondary to posterior urethral valves. The findings on prenatal sonography, postnatal voiding cystourethrography, and magnetic resonance imaging are described.
The effects of propiverine hydrochloride (P-4, CAS 60569-19-9), a new drug to treat pollakiuria, was investigated on the spontaneous contractions of isolated guinea-pig urinary bladder strip and rhythmic urinary bladder contractions of anesthetized dog. At 10(-6)-10(-5) mol/l P-4 raised the base line of an isolated guinea-pig urinary bladder strip and accelerated its spontaneous contraction. At 10(-4) mol/l P-4 raised, and then lowered the baseline, and accelerated then suppressed its spontaneous contractions. Papaverine at 10(-6)-10(-4) mol/l also showed a similar action as P-4 in the isolated guinea-pig urinary bladder strip. Flavoxate at 10(-6)-10(-4) mol/l raised its base line and accelerated its spontaneous contractions. Those of P-4 at 10(-5) mol/l were not inhibited by tetrodotoxin 10(-6) mol/l). At doses of 50 mg/kg or more, intraduodenal administration of P-4 suppressed the frequency of rhythmic urinary bladder contractions of anesthetized dog in a dose-dependent manner. These results indicate that P-4 shows mainly an accelerating action on the endogenous spontaneous contractions of urinary bladder, but on exogenous contractions induced by the Balloon's method it shows an suppressing action and regulates the functions of the urinary bladder, so P-4 might become a useful drug for the clinical treatment of micturitional dysfunction, for example, pollakiuria.
The role of protease-activated receptor-2 (PAR-2) in the regulation of the rat urinary bladder contractility was investigated. Both trypsin and PAR-2 activating peptide (SLIGRL-NH(2)) produced a concentration-dependent contractile response in the urinary bladder preparations. These contractions were abolished by removal of the urinary bladder mucosa and were significantly reduced by indomethacin (10 microM). These results suggest that activation of PAR-2 stimulates release of prostaglandins from mucosal layer and thereby contracts rat urinary bladder smooth muscles.
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Urinary epithelia separate urine from interstitial fluid. In the mammal, this tight epithelium has a limited transport capacity but is capable of moving sodium from urine to blood through an aldosterone-sensitive cellular pathway. In lower vertebrates, absorption of ions and water from the urine can contribute significantly to fluid and electrolyte homeostasis. Transepithelial ion transport and maintenance of cellular composition are interdependent, requiring a balance between movements across the apical and basolateral plasma membranes through a variety of pathways including electrodiffusion through ion channels. A variety of such channels has been identified in urinary epithelia. Apical membranes contain amiloride-sensitive, highly selective sodium channels of low conductance (approximately 5-10 pS). There is evidence that in mammalian bladders trypsin-like enzymes in the urine continually degrade these channels, decrease in cation selectivity being followed by loss of the channels from the membrane. New channels stored in the cytoplasm appear to provide a source for replenishment of the membrane. Other channels of higher conductance and lower selectivity have also been described in both mammalian and amphibian bladders, but their physiological significance remains to be established. Basolateral membranes contain potassium channels. In the mammalian bladder, in which chloride appears to be distributed at electrochemical equilibrium, chloride conductance exceeds potassium conductance and patch clamp studies have revealed a chloride channel of conductance approximately 60 pS detectable immediately on patch excision and active at normal membrane potentials. In the amphibian bladder, a variety of findings indicates the presence of a basolateral membrane chloride conductance, but patch clamp data are not yet available.
The relative importance of bladder distension, urinary pH and sodium ion concentration for cell proliferation in the bladder epithelium of rats fed various sodium salts was investigated. When a diet containing 5% NaHCO3 was fed to male rats, the bladder epithelium showed an increase in replicating cells, together with distension, increased urine pH and high urine sodium ion concentration. Cell proliferation also occurred when bladders were subjected to distension in vivo by mechanical (female) or physiological (male) means. Inclusion of CaCO3 in the diet produced high urinary pH without alteration in the other factors and did not induce cell proliferation. Increased proliferation occurred when CaCO3 was combined with these mechanical or physiological treatments. Thus, high urinary pH was of secondary importance to bladder distension as a causative factor, but acted to enhance cell proliferation when distension occurred. Similar findings were obtained with regard to sodium ion concentration. In conclusion, this study demonstrated that bladder distension is one of the prerequisites for promoter-induced cell proliferation in the bladder epithelium, with high urinary pH and sodium ion concentration.
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Evaluation of the anatomic location of the distended and empty urinary bladders and urethras of healthy adult male and female dogs and cats by retrograde urethrocystography revealed substantial variations. In 15 dogs in lateral recumbency with empty bladder lumens, the caudal portion of the urinary bladder was within the pelvic canal in 5 of 7 male and 5 of 8 female dogs. In female dogs examined in ventrodorsal recumbency, only 4 of 8 had the empty urinary bladders in part within the pelvic canal. After luminal distention, 3 of 7 male and 3 of 8 female dogs, while in lateral recumbency, had the urinary bladders in part intrapelvically. However, when female dogs were placed in ventrodorsal recumbency, only 1 of 7 urinary bladders was in part within the pelvis. The urinary bladders of 14 cats were consistently within the abdominal cavity, irrespective of whether the bladder lumen was distended or empty. Urethral flexures occurred in dogs with intrapelvic bladders that were distended or empty. Urethral flexures were not found in cats. The urethras of dogs and cats in lateral recumbency were generally closer to the floor of the pelvis after urinary bladder distention than when the bladder was empty. The urethra of the dogs and cats in ventrodorsal recumbency was to the left or right of or on the midsagittal plane, whether the urinary bladder was empty or distended. A greater degree of lateral displacement was encountered in ventrodorsal recumbency after urinary bladder distention.
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Spinal cord injury and cyclophosphamide-induced cystitis dramatically alter lower urinary tract function and produce neurochemical, electrophysiological, and anatomical changes that may contribute to reorganization of the micturition reflex. Mechanisms underlying this neural plasticity may involve alterations in neurotrophic factors in the urinary bladder. These studies have determined neurotrophic factors in the urinary bladder that may contribute to reorganization of the micturition reflex following cystitis or spinal cord injury. A ribonuclease protection assay was used to measure changes in urinary bladder neurotrophic factor mRNA (betaNGF, BDNF, GDNF, CNTF, NT-3, and NT-4) following spinal cord injury (acute/chronic) or cyclophosphamide-induced cystitis (acute/chronic). The correlation between urinary bladder nerve growth factor mRNA and nerve growth factor protein expression was also determined. Each experimental paradigm resulted in significant (P </= 0.05-0.005) changes in urinary bladder neurotrophic factor mRNA, although the magnitude of the changes differed between paradigms. Urinary bladders from rats with acute spinal cord injury (4 days) exhibited the largest increase in neurotrophic factor mRNA levels (betaNGF, 21-fold increase; BDNF, 78-fold increase; GDNF, 11-fold increase; CNTF, 5.5-fold increase; NT-3, 10-fold increase; NT-4, 25-fold increase) relative to control urinary bladders. More modest but significant increases were demonstrated for urinary bladders from rats with chronic (4-6 weeks) spinal cord injury. Significant increases in urinary bladder neurotrophic factor mRNA levels of comparable magnitude were demonstrated following either acute or chronic cyclophosphamide-induced cystitis. Increased abundance of urinary bladder nerve growth factor mRNA was not always associated with increased total urinary bladder nerve growth factor. Total urinary bladder nerve growth factor decreased following acute or chronic cystitis despite increased abundance of nerve growth factor mRNA. Urinary bladder nerve growth factor mRNA correlates with protein measures 5-6 weeks following spinal cord injury but not earlier. The 5- to 6-week time point coincided with the reemergence of the spinal bladder-to-bladder reflex mechanisms following spinal cord injury. Discrepancies between two measures (mRNA and protein) may reflect retrograde axonal transport of nerve growth factor to the dorsal root ganglia (L6-S1). Retrogradely transported NGF may play a role in altered lower urinary tract function following spinal cord injury or cyclophosphamide-induced cystitis.
In 54 patients with a superficial transitional cell carcinoma of the bladder urinary (pTa/pTl) apart from a differentiated TUR a quadrant biopsy was investigated in relation to other tumour parameters and the rate of recidivations. Altogether dysplastic changes were to be found in the margin of the tumour in 14 tumours (30%), a positive quadrant biopsy in 20 tumours (37%). Dysplasias in the margin of the tumour without atypias of the remaining mucous membrane were found only in 4 tumours (7%). Dysplasias increase with increasing degree G from 17% in G I tumours to 50% in G III tumours. The rate of recidivations in a control period of 2 years and a chemorecidivation prophylaxis with adriamycin was 14/20 (70%) in positive quadrant biopsy and 6/34 (18%) in negative quadrant biopsy.
We experienced a case of a 60-year-old male with a foreign body in the urinary bladder. He had inserted chewing gum into the urethra for the purpose of masturbation, and it had slipped into the bladder. We collected 1,436 cases of vesico-urethral foreign body from the Japanese literature including our case, and reviewed these cases with some statistical analysis.
The effects of bacillus Calmette-Guerin (BCG) on the cytotoxic activities of peripheral blood lymphocytes against human T24 lined and freshly separated autologous urinary bladder transitional carcinoma cells in patients with urinary bladder cancer were analyzed in a 12-hour chromium 51 (51Cr) release assay. The results of this study indicate that BCG activates the tumor killing system through stimulation of effector cells and elevation of target cell susceptibility in patients with urinary bladder cancer, suggesting that BCG-augmented cytotoxicity may be oriented specifically to urinary bladder cancer cells. This could explain the remarkable clinical benefits of intravesical instillation of BCG against urinary bladder cancer.
Histopathological and angiographic findings were correlated in 6 cases of tuberculosis of the urinary bladder. The number of vessels was only slightly increased in the initial and fibrotic stages, whereas hypervascularization was observed in the exudative and productive stages. Otherwise the angiographic changes were nonspecific. Thus it was not possible to distinguish tuberculous cystitis from cystitis of other genesis, and in some instances from tumours of the urinary bladder either.
The urinary bladder is often involved in an inguinal hernia, but herniation of the entire bladder into the scrotum is rare. As many as 4% of inguinal hernias may involve the bladder, usually in the form of a sliding hernia. Most urinary bladder herniations are diagnosed at the time of inguinal herniorrhaphy, and are therefore most commonly repaired through an inguinal incision. If the diagnosis requires amendment, alternative surgical approaches are available. We studied two patients with massive inguinoscrotal herniation of the urinary bladder, commonly referred to as "scrotal cystocele." We reviewed the literature, incidence, causes, diagnosis, and surgical consideration of herniation of the urinary bladder, and gave particular attention to the interrelationship of bladder herniations with inguinal hernias.
The urinary bladder, as do all smooth muscle organs, depends on the delivery of oxygen and metabolic substrates for proper functioning. Although glucose metabolism has been studied and evaluated for a variety of smooth muscle systems, little is known about carbohydrate metabolism of the urinary bladder. In the present investigation glucose metabolism and glycogen formation of the urinary bladder of the rabbit was studied in vitro. Isolated urinary bladder strips were prepared from bladder base and body and the following metabolic determinations were made: glucose utilization, glycogen formation, CO2, and lactic acid formation. In addition, the effect of insulin on glucose metabolism was investigated. Glucose utilization was similar in bladder base and body (6.57 +/- 0.67 mumols/gm./2 hours in combined tissues). Eighty-one percent of the glucose utilized was metabolized to lactate whereas 11% was oxidized to CO2 and 4.7% was incorporated into glycogen. Insulin caused a small but significant increase in glucose utilization by bladder strips.
PSK, a protein-bound polysaccharide Kureha, was tested for its ability to modulate the cytotoxicity of lymphocytes that act on autologous tumor cells and T24 human urinary bladder tumor cells in urinary bladder cancer patients in a 6-h 51Cr release assay. In vitro treatment of peripheral blood lymphocytes (PBL) with PSK for 18 hours resulted in an augmentation or induction of cytotoxicity against relatively resistant T24 cells in previously reactive and nonreactive cases, respectively. The PSK-treated PBL were able to kill more effectively tumor cells that were freshly isolated from the same cancer patients than non-treated PBL. The effects of PSK were noted with PBL as well as tumor infiltrating lymphocytes (TIL) and with PSK at concentrations of 10 to 100 micrograms./ml., while PSK at higher doses reduced their lytic activities. The addition of PSK to the assay at the same concentrations also enhanced the cytotoxicities. Autologous tumor killing (ATK) activities of both large granular lymphocytes (LGL) and T lymphocytes were enhanced by PSK. Treatment of PBL with PSK did not effect on the proportion of PBL binding to the tumor cells, while it augmented the cytotoxic activity. Cell-free supernatant of PSK-stimulated lymphocyte culture did not contain any detectable amounts of interferon-alpha (IFN-alpha), interferon-gamma (IFN-gamma) and interleukin-2 (IL-2). In addition, anti-IFN-alpha monoclonal antibody (MAb), anti-IFN-gamma MAb and anti-IL-2 MAb did not inhibit PSK-induced augmentation of cytotoxicity against T24. Oral administration of PSK (three gm./day) to patients with urinary bladder cancer daily for seven days before operation resulted in an augmentation of the cytotoxicity against T24 cells in five out of 10 patients and no change of the cytotoxicity in the other five patients. ATK activity was also enhanced by oral administration of PSK in three out of five patients. These results indicate that the antitumor activity of PSK may be in part mediated through activation of tumor killing system independent of IFN-alpha, IFN-gamma and IL-2.