Roles of polyuria and hyperglycemia in bladder dysfunction in diabetes.
Roles of polyuria and hyperglycemia in bladder dysfunction in diabetes.
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DOI：
10.1016/j.juro.2012.08.222
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发表时间：
2013-03
影响因子：
6.6
通讯作者：
Liu, Guiming
中科院分区：
文献类型：
--
作者：
Xiao, Nan;Wang, Zhiping;Huang, Yexiang;Daneshgari, Firouz;Liu, Guiming
Diabetes mellitus (DM) causes diabetic bladder dysfunction (DBD). We aimed to identify the pathogenic roles of polyuria and hyperglycemia on DBD in rats. 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. 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. 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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影响因子：
6.6
作者：
Daneshgari, Firouz;Liu, Guiming;Imrey, Peter B.
通讯作者：
Imrey, Peter B.
影响因子：
--
作者：
Searls Y;Smirnova IV;Vanhoose L;Fegley B;Loganathan R;Stehno-Bittel L
通讯作者：
Stehno-Bittel L
影响因子：
2.1
作者：
Beshay, E;Carrier, S
通讯作者：
Carrier, S
影响因子：
6.6
作者：
Deveaud, CM;Macarak, EJ;Howard, PS
通讯作者：
Howard, PS
影响因子：
4.3
作者：
Stevenson, K;Kucich, U;Howard, PS
通讯作者：
Howard, PS