A New Technique to Repair Vesicorectal Fistula: Overlapping Rectal Muscle Plasty by Transanal Endoscopic Surgery.

OBJECTIVE: To evaluate clinical results of a novel surgical technique, we developed to repair vesicorectal fistula (VRF) occurring after prostatectomy, hospital records of the patients, who underwent the new surgical treatment, were assessed. METHODS: The novel surgical technique is called "overlapping rectal muscle plasty," which is performed under transanal endoscopic microsurgery (TEM). During the new procedure, a complete fistulectomy was first performed, and then the proper muscle layer of the rectum was folded, overlapped, and sutured to create a thick wall between the rectum and urinary bladder. This operation was carried out in 15 patients with VRF following radical prostatectomy. RESULTS: The operation was safely performed in all patients with an average time of 127.2 min. Fistula was corrected in 13 patients (86.7%), who were then freed from both urinary and intestinal diversions. CONCLUSIONS: Overlapping rectal muscle plasty by TEM is a safe procedure. The success rate seems to be acceptable in selected patients. This new repair method may be considered as a minimally invasive option in the surgical treatment of VRF after prostatectomy.

A case series of pelvic fracture patients who developed lower urinary tract symptoms after transarterial embolization of bilateral internal iliac arteries.

Cases: Transarterial embolization of bilateral internal iliac arteries (TAE) is a useful hemostatic method for the management of pelvic fracture patients, but its effects on urinary functions remain unclear. In this study, we evaluated the impact of TAE on lower urinary tract symptoms (LUTS) in 10 pelvic fracture patients. Outcomes: Lower urinary tract symptoms before and after hospitalization were evaluated by International Prostate Symptoms Score, Overactive Bladder Symptoms Score, and Quality Of Life score. All scores showed significant worsening. The changes did not correlate with sex, age, injury severity score, or durations of unstable hemodynamics or urethral catheterization. Changes of International Prostate Symptoms Score and Quality Of Life score showed significant positive correlations with intervals between the evaluations. Conclusion: Pelvic fracture patients treated with TAE showed significant worsening of LUTS. Risk for exacerbation of LUTS should be taken into consideration when deciding to use TAE.

Effects of silodosin, a selective α1A-adrenoceptor antagonist, on bladder blood flow and bladder function in a rat model of atherosclerosis induced chronic bladder ischemia without bladder outlet obstruction.

PURPOSE: We investigated the effects of the selective α1A-adrenoceptor antagonist silodosin on bladder blood flow and bladder function in a rat model of atherosclerosis induced chronic bladder ischemia without bladder outlet obstruction. MATERIALS AND METHODS: The chronic bladder ischemia model was prepared by creating balloon endothelial injury of the bilateral iliac arteries in male rats. Using an osmotic pump, chronic bladder ischemia rats received silodosin subcutaneously at a rate of 0.1 or 0.3 mg/kg per day, or vehicle for 8 weeks. All groups received a 2% cholesterol diet throughout the experiment. For each α1-adrenoceptor subtype mRNA expression in bladder microvessels was examined by in situ hybridization. Bladder blood flow was measured using a laser speckle blood flow imager. Malondialdehyde in bladder tissue and 8-hydroxy-2'-deoxyguanosine in urine were measured as markers of oxidative stress. A metabolic cage study and cystometry were performed in conscious rats. RESULTS: The expression of all α1-adrenoceptor subtype mRNA was observed in rat bladder microvessels. Silodosin abrogated the decreased bladder blood flow in the empty bladder and during bladder distention that were evident in rats with chronic bladder ischemia. Levels of oxidative stress markers in these rats were significantly decreased by silodosin administration. Silodosin ameliorated bladder dysfunction in rats with chronic bladder ischemia in the metabolic cage study and on cystometry. CONCLUSIONS: Results suggest that in ischemic conditions α1-adrenoceptor antagonists such as silodosin may improve bladder function by restoring bladder blood flow.

Impaired detrusor contractility in a rat model of chronic bladder ischemia.

OBJECTIVE: To examine the effect of chronic ischemia associated with vascular disorders on bladder function, we investigated bladder contractility and changes in morphology and nerve distribution in a rat model of chronic bladder ischemia. METHODS: Adult male Sprague-Dawley rats were divided into arterial endothelial injury, sham, and control groups. The injury group underwent balloon endothelial injury of the iliac arteries and received a 2% cholesterol diet. The sham group was only incised bilaterally in the inguinal region and received the 2% cholesterol diet. The control group did not undergo any procedure and received a regular diet (0.09% cholesterol). All animals were euthanized after 8 weeks. Bladders were removed and weighed, and sections were used for muscle strip contraction and histologic analyses. Cross-sections of dissected common iliac arteries were examined histologically. RESULTS: Bladder contractile response and tension were significantly decreased in the injury group compared with the sham and control groups. Tissue from the injury group exhibited marked arterial occlusion with wall thickening. In the injury group, the collagen and muscle ratio (0.80 ± 0.12) was significantly greater than in the control (P = .01) and sham (P = .04) groups. Significantly fewer protein gene product 9.5 (PGP9.5)-positive nerve fibers were found in the injury group (513 ± 53) than in the control (P = .01) and sham (P = .03) groups. CONCLUSION: Vascular occlusive disorders cause fibrosis and reduce the number of nerves innervating the bladder, which leads to decreased bladder contractility in a rat model of chronic bladder ischemia.

Suppression of bladder overactivity and oxidative stress by the phytotherapeutic agent, Eviprostat, in a rat model of atherosclerosis-induced chronic bladder ischemia.

OBJECTIVES: To clarify the mechanism by which chronic bladder ischemia causes bladder functional changes, and to investigate the involvement of oxidative stress and pro-inflammatory cytokines, and the effects of the phytotherapeutic drug, Eviprostat, on these biochemical marker levels and bladder function. METHODS: Male Sprague-Dawley rats aged 15 weeks were divided into three groups. Arterial injury was experimentally induced by balloon endothelial injury of the iliac arteries, and a 2% cholesterol diet was given for 8 weeks. Rats in the arterial-injury group were given daily oral vehicle or Eviprostat, whereas sham-operated animals on a regular diet (0.09% cholesterol) were given vehicle for the last 2 weeks. Eight weeks after surgery, the levels of bladder pro-inflammatory cytokines, as well as bladder and urinary oxidative-stress markers, were determined. Cystometrograms were carried out without anesthesia or restraint. RESULTS: Bladder and urinary oxidative-stress markers, and bladder pro-inflammatory cytokine levels were significantly increased in the arterial-injury group, and Eviprostat markedly suppressed these increase. The cystometrograms showed that arterial injury decreased the intermicturition interval without affecting the micturition pressure. This decrease was reversed by Eviprostat treatment. CONCLUSIONS: Oxidative stress and pro-inflammatory cytokines might be involved in the development of overactive bladder by atherosclerosis-induced chronic bladder ischemia. Eviprostat might provide an attractive treatment option for individuals with bladder dysfunction due to chronic bladder ischemia because of its anti-oxidant and anti-inflammatory properties.

Involvement of angiotensin II type 1 receptor on pathological remodeling and dysfunction in obstructed bladder.

OBJECTIVES: To determine whether long-term administration of an angiotensin II type 1 receptor antagonist improves morphology and function in obstructed bladders. METHODS: Male Sprague-Dawley rats underwent surgery to produce bladder outlet obstruction (bladder outlet obstruction group; n = 32) or sham surgery (sham group; n = 16). A total of 2 weeks later, 16 bladder outlet obstruction-rats were given the AT1 antagonist, candesartan, subcutaneously (candesartan group) using an osmotic pump for 4 weeks; the remaining bladder outlet obstruction-rats received vehicle (bladder outlet obstruction group). A total of 6 weeks after surgery, we compared continuous cystometry, bladder weight, strip contraction, histology and messenger ribonucleic acid expression of growth factors, nicotinamide adenine dinucleotide phosphate oxidase 1 and renin-angiotensin system components among the three groups. RESULTS: Bladder weights markedly increased with bladder outlet obstruction (578 ± 159 mg), and candesartan (344 ± 111 mg) suppressed this increase. Micturition pressure, which was significantly higher with bladder outlet obstruction, was unaffected by candesartan. The shortened micturition interval and decreased micturition volume with bladder outlet obstruction were significantly prolonged and increased by candesartan. Candesartan also significantly decreased residual urine. Histologically, the collagen fiber-to-muscle ratio was significantly increased with bladder outlet obstruction (0.85 ± 0.25) compared with the sham group (0.53 ± 0.18); this increase was suppressed by candesartan (0.49 ± 0.21). The messenger ribonucleic acid expression of heparin-binding epidermal growth factor-like growth factor, transforming growth factor-ß1 and nicotinamide adenine dinucleotide phosphate oxidase 1 significantly increased with bladder outlet obstruction, but it was significantly reduced by candesartan. Compared with the bladder outlet obstruction group, candesartan increased the maximal contraction of bladder strips for all stimuli except for angiotensin II. CONCLUSION: These findings suggest that bladder angiotensin II type 1 receptors contribute to the pathophysiology of remodeling and dysfunction in obstructed bladder.

The effect of atherosclerosis-induced chronic bladder ischemia on bladder function in the rat.

AIMS: To develop a rat model of atherosclerosis-induced chronic bladder ischemia and investigate the effect of chronic bladder ischemia on voiding behavior and bladder function. METHODS: Adult male rats were divided into three groups. The arterial injury (AI) group underwent endothelial injury of the iliac arteries and received a 2% cholesterol diet. The sham group underwent sham operation and received a 2% cholesterol diet. The control group received a regular diet. After 8 weeks, a metabolic cage study and cystometry were performed without anesthesia. Bladder blood flow was measured using a laser Doppler blood flowmeter. Histological examination of the iliac arteries and the bladder was performed. The bladder was also processed for immunohistochemical staining of oxidative stress markers. RESULTS: The metabolic cage study showed that in the AI group, voiding frequency significantly increased while voided volume significantly decreased. Cystometry showed that the frequency of reflex bladder contractions was significantly higher in the AI group. Filling-induced decrease in bladder blood flow was the greatest in the AI group. Histological study showed that in the AI group alone, atherosclerotic occlusion occurred in the iliac arteries as well as in the downstream bladder microvessels. Oxidative stress marker positive cells were more prevalent in the AI bladder than in the other bladders. CONCLUSIONS: Combined with a high-cholesterol diet, endothelial injury of iliac arteries induced arterial occlusive disease in the downstream vessels and consequent bladder ischemia in rats. This model of chronic bladder ischemia showed detrusor overactivity manifested as an increase in voiding frequency.

Increased bladder activity is associated with elevated oxidative stress markers and proinflammatory cytokines in a rat model of atherosclerosis-induced chronic bladder ischemia.

AIMS: To further characterize, in a rat model, the effects of atherosclerosis-induced chronic bladder ischemia on bladder function and associated changes in oxidative stress markers and proinflammatory cytokines. METHODS: Adult Sprague-Dawley male rats were divided into three groups (arterial endothelial injury: AI, sham, naïve). The AI group (n = 14) underwent endothelial injury of the iliac arteries and received a 2% cholesterol diet. The sham group (n = 12) underwent sham operation and received a 2% cholesterol diet. The naïve group (n = 12) received a regular diet. After 8 weeks, cystometrograms (CMG) without anesthesia or restraint were performed. In bladders from each group, oxidative stress markers (8-hydroxy-2'-deoxyguanosine: 8-OHdG; malondialdehyde: MDA) and proinflammatory cytokines (IL-8 like cytokine CXCL1/CINC-1, TNF-α, IL-6) were quantified. Histological examination of the iliac arteries was also performed. RESULTS: At 8 weeks, the body and bladder wet weights were not significant different among the three groups. The micturition interval in the AI group decreased significantly compared with those in the other two groups, but maximum pressure during micturition did not change. The iliac arteries in the AI group revealed thickening of intima as well as diffuse media fibrosis at the sites of balloon injury. The levels of oxidative stress markers and proinflammatory cytokines were significantly higher in the AI than in the other groups. CONCLUSION: Oxidative stress and inflammation may be key factors in the development of bladder overactivity in atherosclerosis-induced chronic bladder ischemia.