Pressure-flow studies in patients with benign prostatic hyperplasia: a study comparing suprapubic and transurethral methods.
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AIM: To compare the use of the suprapubic puncture method versus the transurethral method in pressure-flow studies in patients with benign prostatic hyperplasia. METHODS: Twenty-three men with benign prostatic hyperplasia underwent both suprapubic and transurethral pressure-flow studies during a single session. Standard pressure-flow variables were recorded in all patients with both methods, enabling calculation of obstruction using commonly used grading systems, such as the urethral resistance algorithm, the Abrams-Griffith (AG) number and the Schaer linear nomogram. RESULTS: There were statistically significant differences between the methods in the mean values of maximum flow rate (P < 0.05), detrusor pressure at the maximum flow (P < 0.01), urethral resistance algorithm (P < 0.01), AG number (P < 0.01) and maximum cystic capacity (P < 0.01). Of the men in the study, 10 (43.5%) remained in the same Schaer class with both methods and 18 (78.3%) in the same AG number area. Using the transurethral method, 12 (52.2%) men increased their Schaer class by one and 1 (4.3%) by two. There were also differences between the suprapubic and transurethral methods using the AG number: 4 (17.4%) men moved from a classification of equivocal to obstructed and 1 (4.3%) from unobstructed to equivocal. CONCLUSION: The differences between the techniques for measuring intravesical pressure alter the grading of obstruction determined by several of the commonly used classifications. An 8 F transurethral catheter significantly increases the likelihood of a diagnosis of bladder outlet obstruction when compared with the suprapubic method. (+info)
Regulation of bladder muscarinic receptor subtypes by experimental pathologies.
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1 The M3 muscarinic receptor subtype is widely accepted as the receptor on smooth muscle cells that mediates cholinergic contraction of the normal urinary bladder and other smooth muscle tissues, however, we have found that the M2 receptor participates in contraction under certain abnormal conditions. The aim of this study was to determine the effects of various experimental pathologies on the muscarinic receptor subtype mediating urinary bladder contraction. 2 Experimental pathologies resulting in bladder hypertrophy (denervation and outlet obstruction) result in an up-regulation of bladder M2 receptors and a change in the receptor subtype mediating contraction from M3 towards M2. Preventing the denervation-induced bladder hypertrophy by urinary diversion prevents this shift in contractile phenotype indicating that hypertrophy is responsible as opposed to denervation per se. 3 The hypertrophy-induced increase in M2 receptor density and contractile response is accompanied by an increase in the tissue concentrations of mRNA coding for the M2 receptor subtype, however, M3 receptor protein density does not correlate with changes in M3 receptor tissue mRNA concentrations across different experimental pathologies. 4 This shift in contractile phenotype from M3 towards M2 subtype is also observed in aged male Sprague-Dawley rats but not females or either sex of the Fisher344 strain of rats. 5 Four repeated, sequential agonist concentration response curves also cause this shift in contractile phenotype in normal rat bladder strips in vitro, as evidenced by a decrease in the affinity of the M3 selective antagonist p-fluoro-hexahydro-sila-diphenidol (p-F-HHSiD). 6 A similar decrease in the contractile affinity of M3 selective antagonists (darifenacin and p-F-HHSiD) is also observed in bladder specimens from patients with neurogenic bladder as well as certain organ transplant donors. 7 It is concluded that although the M3 receptor subtype predominantly mediates contraction under normal circumstances, the M2 receptor subtype can take over a contractile role when the M3 subtype becomes inactivated by, for example, repeated agonist exposures or bladder hypertrophy. This finding has substantial implications for the clinical treatment of abnormal bladder contractions. (+info)
Inhibition of EGFR signaling abrogates smooth muscle proliferation resulting from sustained distension of the urinary bladder.
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Urinary bladder outlet obstruction results in sustained stretch of the detrusor muscle and can lead to pathological smooth muscle hyperplasia and hypertrophy. The epidermal growth factor receptor (EGFR) is a cognate receptor for mitogens implicated in bladder hyperplasia/hypertrophy. Here, we investigated the potential for modulation of this pathway by pharmacologic targeting with a clinically available EGFR antagonist using an organ culture model of bladder stretch injury as a test system. Urinary bladders from adult female rats were distended in vivo with medium containing the EGFR inhibitor ZD1839 (gefitinib, Iressa). The bladders were excised and incubated in ex vivo organ culture for 4-24 h. EGFR phosphorylation, DNA proliferation, and the extent of apoptosis in the cultured tissues were assessed. To verify that the smooth muscle cells (SMC) are a target of the EGFR inhibitor, primary culture human and rat bladder SMC were subjected to cyclic mechanical stretch in vitro in the presence of ZD1839. Levels of phosphorylated EGFR were significantly increased in the detrusor muscle with 12 h of stretch in the organ cultures. This activation coincided with a subsequent 23-fold increase in DNA synthesis and a 30-fold decrease in apoptosis in the muscle compartment at 24 h. In the presence of ZD1839, DNA synthesis was reduced to basal levels without an increase in the rate of apoptosis under ex vivo conditions. Mechanical stretch of bladder SMC in vitro resulted in a significant increase in DNA synthesis, which was completely abrogated by treatment with ZD1839 but not by AG825, an inhibitor of the related receptor, ErbB2. Our results indicate that the EGFR pathway is a physiologically relevant signaling mechanism in hypertrophic bladder disease resulting from mechanical distension and may be amenable to pharmacologic intervention. (+info)
Infective arthritis secondary to bladder outflow obstruction.
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We describe two cases of septic arthritis occurring in association with lower urinary tract infection in elderly men. In both cases the organism isolated from both the joint and the urine was Staphylococcus aureus. Further investigation of the urinary tract in both individuals identified bladder outflow obstruction secondary to benign prostatic hyperplasia predisposing them to infection. The urinary tract should be suspected as a focus of infection in septic arthritis in elderly men and further investigation of the urinary system may disclose a surgically correctable lesion. (+info)
Postoperative retention of urine: a prospective urodynamic study.
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OBJECTIVE: To investigate the cause of post-operative retention of urine in elderly men. DESIGN: Prospective study. SETTING: Northern General Hospital, Sheffield. PATIENTS: 32 consecutive men (median age 73, range 55-85) referred to the urology department who were unable to pass urine either within 48 hours after operation and required catheterisation (23) or after removal of a catheter inserted at the initial operation (nine). INTERVENTION: Intermittent self catheterisation. MAIN OUTCOME MEASURES: Urological investigation by medium fill and voiding cystometry within four weeks after operation, and minimum follow up three months thereafter. RESULTS: 6 patients resumed normal voiding before urodynamic assessment, three proceeded straight to prostatectomy, and one was unfit for self catheterisation. Of 22 men who underwent urodynamic investigation, only five had bladder outflow obstruction, who subsequently had successful prostatectomy; 15 showed either a low pressure-low flow system (seven) or complete detrusor failure (eight) and two showed pelvic parasympathetic nerve damage. With intermittent self catheterisation spontaneous voiding returned in all but one man within a median of 8 weeks (range 6-32 weeks). Recovery of bladder function took significantly longer in men with detrusor failure than in those with an underactive bladder (median 10 weeks (range 6-32 weeks) v median 8 weeks (range 6-8 weeks); p = 0.05). Three months later all patients had re-established their own normal voiding pattern with minimal residual urine on ultrasonography and satisfactory flow rates. CONCLUSIONS: Postoperative urinary retention in elderly men is not an indication for prostatectomy; a normal pattern of micturition can be re-established by intermittent self catheterisation in most men. (+info)
A gap junction blocker inhibits isolated whole bladder activity in normal rats and rats with partial bladder outlet obstruction.
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We examined the effect of 18alpha-glycyrrhetinic acid (18alpha-GA), a gap junction blocker, or propiverine hydrochloride on the activity of isolated whole bladders obtained from intact rats and rats with partial bladder outlet obstruction (BOO). Thirty-two female Sprague-Dawley rats were divided into an intact group and a BOO group. The whole bladder was harvested from each rat and isovolumetric cystometry was performed in Krebs solution. Changes of bladder activity were recorded after addition of 18alpha-GA or propiverine hydrochloride to the perfusate. Propiverine hydrochloride inhibited the amplitude and duration of contraction in both intact and BOO groups. Propiverine hydrochloride also reduced the baseline bladder pressure in the BOO group, but not in the intact group. In contrast, 18alpha-GA inhibited the amplitude and duration of bladder contraction, and also reduced the baseline pressure, in both intact and BOO groups. BOO bladders showed inhibition of the amplitude and duration of bladder contraction at lower concentrations of 18alpha-GA than intact bladders. A gap junction blocker suppressed the in vitro activity of BOO bladders more effectively than that of intact bladders. Therefore, inhibition of intercellular communication in the bladder via gap junctions may be useful for treating detrusor overactivity, as well as propiverine hydrochloride. (+info)
Involvement of STAT3 in bladder smooth muscle hypertrophy following bladder outlet obstruction.
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We examined the involvement of the signal transducer and activator of transcription 3 (STAT3) in bladder outlet obstruction (BOO)-induced bladder smooth muscle hypertrophy using a rat in vivo and in vitro study. BOO induced increases in bladder weight and bladder smooth muscle thickness 1 week after the operation. By using antibody microarrays, 64 of 389 proteins blotted on the array met our selection criteria of an INR value between > or = 2.0 and < or = 0.5. This result revealed up-regulation of transcription factors, cell cycle regulatory proteins, apoptosis-associated proteins and so on. On the other hand, down-regulation (INR value < or = 0.5) of proteins was not found. In a profiling study, we found an increase in the expression of STAT3. A significant increase in nuclear phosphorylated STAT3 expression was confirmed in bladder smooth muscle tissue by immunohistochemistry and Western blot analysis. Cyclical stretch-relaxation (1 Hz) at 120% elongation significantly increased the expression of STAT3 and of alpha-smooth muscle actin in primary cultured bladder smooth muscle cells. Furthermore, the blockade of STAT3 expression by the transfection of STAT3 small interfering RNA (siRNA) significantly prevented the stretch-induced increase in alpha-smooth muscle actin expression. These results suggest that STAT3 has an important role in the induction of bladder smooth muscle hypertrophy. (+info)
Stereological study of collagen and elastic system in the detrusor muscle of bladders from controls and patients with infravesical obstruction.
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OBJECTIVE: Compare detrusor muscle of normal and patients with infravesical obstruction, quantifying the collagen and elastic system fibers. MATERIALS AND METHODS: We studied samples taken from bladders of 10 patients whose ages ranged from 45 to 75 years (mean = 60 years), who underwent transvesical prostatectomy for treatment of BPH. Control material was composed of 10 vesical specimens, removed during autopsies performed in cadavers of accident victims, with ages between 18 and 35 years (mean = 26 years). RESULTS: The results of collagen and elastic fibers quantification (volumetric density) demonstrated the following results in percentage (mean +/- standard deviation): collagen in BPH patients = 4.89 +/- 2.64 and 2.32 +/- 1.25 in controls (p < 0.0001), elastin in BPH patients = 10.63% +/- 2.00 and 8.94% +/- 1.19 in controls (p < 0.0001). CONCLUSION: We found that the components of connective tissue, collagen and elastic system fibers are increased in the detrusor muscle of patients with infravesical obstruction, when compared to controls. (+info)