Temporal Morphological and Functional Impact of Complete Urinary Diversion on the Bladder: A Model of Bladder Disuse in Rats

Liu, Guiming; Lin, Yun-Hsuan; Li, Mei; Xiao, Nan; Daneshgari, Firouz

doi:10.1016/j.juro.2010.06.090

Cited by 10 publications

(11 citation statements)

References 28 publications

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“…Catheter implantation was carried out as we described previously. 15 The bladder was exposed and a circular purse string suture of 6-0 silk was placed on the bladder wall. A small incision was made in the bladder wall and the catheter (PE-50 tubing with a flared tip) was implanted; a purse string suture was tightened around the catheter.…”

Section: Suprapubic Bladder Catheter Implantation and Conscious Cmg Mmentioning

confidence: 99%

Short‐term diabetes‐ and diuresis‐induced alterations of the bladder are mostly reversible in rats

et al. 2015

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Abbreviations & Acronyms CMG = cystometrogram Con 3w = 3 weeks agematched controls Con 11w = 11 weeks agematched controls DBD = diabetic bladder dysfunction DIU = 5% sucrose-induced diuresis DIU 3w = 3 weeks after 5% sucrose-induced diuresis DIU 3 + 8w = 3 weeks after 5% sucrose-induced diuresis followed by 5% sucrose removal for 8 weeks DIU 11w = 11 weeks after 5% sucrose-induced diuresis DM = diabetes mellitus DM 3w = 3 weeks after streptozotocin-induced diabetes mellitus DM 3 + 8w = 3 weeks after streptozotocin-induced diabetes mellitus followed by insulin replacement treatment for 8 weeks DM 11w = 11 weeks after streptozotocin-induced diabetes mellitus HbA1c = glycated hemoglobin A1c STZ = streptozotocin Objectives: To determine whether diabetes mellitus-and diuresis-induced alterations in the bladder can be reversed in rats. Methods: Male Sprague-Dawley rats were randomly distributed into eight groups (n = 16 per group): 3 weeks and 11 weeks age-matched controls, 3 weeks and 11 weeks after streptozotocin-induced diabetes mellitus, 3 weeks after diabetes mellitus induction then treated with insulin for 8 weeks, 3 weeks and 11 weeks after 5% sucrose-induced diuresis, and 3 weeks after 5% sucrose-induced diuresis followed by removal of 5% sucrose for 8 weeks. Bodyweight, blood glucose and glycated hemoglobin A1c were monitored. At the designated time-points, 24-h urinary habits were examined, and cystometry was carried out in half of the animals. The bladders from the remaining animals were harvested for histological examination, and quantification of smooth muscle, urothelium and collagen components. Results: Insulin treatment reversed hyperglycemia and polyuria in diabetic animals successfully, which was shown by normalization of blood glucose, glycated hemoglobin A1c and 24-h urinary habits. Subsequently, bodyweight, bladder weight and percentage change of bladder components (smooth muscle, collagen, urothelium) in total bladder crosssectional area were reversed to almost normal levels, and the bladder dysfunction was mostly reversed by 8 weeks of glycemic control, seen in the cystometry study. Similar alterations and reversed effects were seen in diuretic rats without and with 5% sucrose removal, respectively. Conclusions: Short-term (3-week induction) diabetes-and polyuria-induced functional and morphological alterations of the bladder can mostly be reversed in rats.Key words: bladder, diabetes, insulin, morphology, smooth muscle. IntroductionDBD, a collective description of clinical symptoms, including decreased sensation, increased capacity, poor emptying 1 and detrusor overactivity, 2 is among the most common and costly complications of DM.3 It is estimated that DBD occurs in approximately 87% of individuals diagnosed with DM, a higher rate than that of widely recognized complications such as neuropathy (60%) and nephropathy (50%).1,3 Although DBD is not life threatening, it substantially affects quality of life. 4The classic symptoms of untreated DM are loss of weight, polyuria, polydipsia and polypha...

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Section: Suprapubic Bladder Catheter Implantation and Conscious Cmg Mmentioning

confidence: 99%

Short‐term diabetes‐ and diuresis‐induced alterations of the bladder are mostly reversible in rats

et al. 2015

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“…UD or sham procedures were performed 10d prior to administering STZ injection, 5% sucrose water, or STZ vehicle (citrate buffer). UD was performed by surgical ureterovaginostomy as described recently by us 11 . The sham procedure included laparotomies and the identification of ureters.…”

Section: Methodsmentioning

confidence: 99%

“…UD was performed by surgical disconnection of the ureters from the bladder and implantation to the uterine cervix as described previously by us 11 . The ureters were identified and ligated distally.…”

Section: Methodsmentioning

confidence: 99%

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Roles of Polyuria and Hyperglycemia in Bladder Dysfunction in Diabetes

et al. 2013

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Purpose Diabetes mellitus (DM) causes diabetic bladder dysfunction (DBD). We aimed to identify the pathogenic roles of polyuria and hyperglycemia on DBD in rats. Materials and Methods Seventy-two female Sprague-Dawley rats were divided: age-matched controls (control), sham urinary diversion (sham), urinary diversion (UD), streptozotocin-induced diabetes after sham UD (DM), streptozotocin-induced diabetes after UD (UD+DM), and 5% sucrose-induced diuresis after sham UD (DIU). UD was performed by ureterovaginostomy 10d before DM induction. Animals were evaluated 20 wks after DM or diuresis induction. We measured 24-hr drinking and voiding volumes and cystometry (CMG). Bladders were harvested for quantification of smooth muscle, urothelium, and collagen. We measured nitrotyrosine and manganese superoxide dismutase (MnSOD) in bladder. Results Diabetes and diuresis caused increases in drinking volume, voiding volume and bladder weight. Bladder weights decreased in the UD and UD+DM groups. Intercontractile intervals, voided volume, and compliance increased in the DIU and DM groups, decreased in the UD, and further decreased in the UD+DM group. The total cross-sectional tissue, smooth muscle and urothelium areas increased in the DIU and DM groups, and decreased in the UD and UD+DM groups. As percentages of total tissue area, collagen decreased in the DIU and DM groups, and increased in the UD and UD+DM groups, and smooth muscle and urothelium decreased in the UD and UD+DM groups. Nitrotyrosine and MnSOD increased in DM and UD+DM rats. Conclusions Polyuria induced bladder hypertrophy, while hyperglycemia induced substantial oxidative stress in the bladder, which may play a pathogenic role in late stage DBD.

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“…4 Structural and functional analyses of the defunctionalization and refunctionalization of the urinary bladder have been previously reported in several animal studies using rabbit or rat models. [5][6][7] However, the bladder refunctionalization model that incorporates urine reperfusion through the reanastomosis of the ureter is challenging, as it is difficult to perform ureteral surgery on rabbits and rats. 5,6 Moreover, neither the gene nor the protein expression related to the structural and functional changes that occur during the defunctionalizing and refunctionalizing of the urinary bladder nor the molecular mechanisms resulting in these phenomena have been investigated.…”

Section: Introductionmentioning

confidence: 99%

Candidate genes involved in the defunctionalization and refunctionalization of the urinary bladder induced by bladder anuria and reperfusion

Kisou

Inoue

Nishijima

et al. 2020

Neurourology and Urodynamics

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Aims We develop a novel rabbit urinary diversion model of bladder defunctionalization due to bladder anuria followed by refunctionalization due to urine reperfusion to investigate the molecular biological background. To validate the results, we used reverse transcription‐polymerase chain reaction (RT‐PCR) to analyze human specimens from defunctionalized bladders in patients receiving dialysis before kidney transplantation. Methods Female rabbits were divided into three groups: control, defunctionalized, and refunctionalized. The bilateral ureters were anastomosed to vagina in the defunctionalized and refunctionalized groups at 0 weeks. In the refunctionalized group, the unilateral ureter was reanastomosed to the bladder at 8 weeks. Results The capacity and compliance of the rabbit bladder in the refunctionalized group were significantly lower than those in the control group at 8 weeks and higher than those in the defunctionalized group at 14 weeks. The significant downregulation of IGFBP2, UPK1B, and CST6 in the defunctionalized group compared with that in the control groups, and the significant downregulation of AGTR2 in the refunctionalized group compared with that in the defunctionalized group in the rabbit bladder‐muscle DNA microarray were validated by RT‐PCR. Human bladder muscle indicated significant downregulation of UPK1B and CST6 and significant downregulation of IGFBP2 in the defunctionalized group, which is consistent with both rabbit bladder‐muscle DNA microarray and rabbit bladder RT‐PCR results. Conclusions The present study using novel model of bladder defunctionalization followed by refunctionalization indicated the consistent downregulation of UPK1B and CST6 in muscle and the consistent downregulation of IGFBP2 in mucosa in process of bladder defunctionalization, which was validated by human specimens.

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Temporal Morphological and Functional Impact of Complete Urinary Diversion on the Bladder: A Model of Bladder Disuse in Rats

Cited by 10 publications

References 28 publications

Short‐term diabetes‐ and diuresis‐induced alterations of the bladder are mostly reversible in rats

Short‐term diabetes‐ and diuresis‐induced alterations of the bladder are mostly reversible in rats

Roles of Polyuria and Hyperglycemia in Bladder Dysfunction in Diabetes

Candidate genes involved in the defunctionalization and refunctionalization of the urinary bladder induced by bladder anuria and reperfusion

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