Department of Urology, Second Hospital of Lanzhou University, Lanzhou, People's Republic of China.
J Urol. 2013 Mar;189(3):1130-6. doi: 10.1016/j.juro.2012.08.222. Epub 2012 Oct 8.
Diabetes mellitus causes diabetic bladder dysfunction. We identified the pathogenic roles of polyuria and hyperglycemia in diabetic bladder dysfunction in rats.
A total of 72 female Sprague-Dawley® rats were divided into 6 groups, including age matched controls, and rats with sham urinary diversion, urinary diversion, streptozotocin induced diabetes mellitus after sham urinary diversion, streptozotocin induced diabetes mellitus after urinary diversion and 5% sucrose induced diuresis after sham urinary diversion. Urinary diversion was performed by ureterovaginostomy 10 days before diabetes mellitus induction. Animals were evaluated 20 weeks after diabetes mellitus or diuresis induction. We measured 24-hour drinking and voiding volumes, and cystometry. Bladders were harvested to quantify smooth muscle, urothelium and collagen. We measured nitrotyrosine and Mn superoxide dismutase in the bladder.
Diabetes and diuresis caused increases in drinking and voiding volume, and bladder weight. Bladder weight decreased in the urinary diversion group and the urinary diversion plus diabetes group. The intercontractile interval, voided volume and compliance increased in the diuresis and diabetes groups, decreased in the urinary diversion group and further decreased in the urinary diversion plus diabetes group. Total cross-sectional tissue, smooth muscle and urothelium areas increased in the diuresis and diabetes groups, and decreased in the urinary diversion and urinary diversion plus diabetes groups. As a percent of total tissue area, collagen decreased in the diuresis and diabetes groups, and increased in the urinary diversion and urinary diversion plus diabetes groups. Smooth muscle and urothelium decreased in the urinary diversion and urinary diversion plus diabetes groups. Nitrotyrosine and Mn superoxide dismutase increased in rats with diabetes and urinary diversion plus diabetes.
Polyuria induced bladder hypertrophy, while hyperglycemia induced substantial oxidative stress in the bladder, which may have a pathogenic role in late stage diabetic bladder dysfunction.
糖尿病会导致糖尿病膀胱功能障碍。我们在大鼠模型中确定了多尿和高血糖在糖尿病膀胱功能障碍中的致病作用。
总共 72 只雌性 Sprague-Dawley®大鼠被分为 6 组，包括年龄匹配的对照组，假导尿组、导尿组、假导尿后链脲佐菌素诱导的糖尿病组、导尿后链脲佐菌素诱导的糖尿病组和假导尿后 5%蔗糖诱导的利尿组。糖尿病诱导前 10 天进行导尿。糖尿病或利尿诱导后 20 周评估动物。我们测量了 24 小时的饮水量和排尿量，并进行了膀胱测压。收集膀胱以定量平滑肌、尿路上皮和胶原。我们测量了膀胱中的硝基酪氨酸和 Mn 超氧化物歧化酶。
糖尿病和利尿导致饮水量和排尿量以及膀胱重量增加。导尿组和导尿加糖尿病组的膀胱重量下降。利尿组和糖尿病组的收缩间期、排尿量和顺应性增加，导尿组减少，导尿加糖尿病组进一步减少。利尿组和糖尿病组的总组织横截面积、平滑肌和尿路上皮面积增加，导尿组和导尿加糖尿病组减少。作为总组织面积的百分比，胶原在利尿组和糖尿病组中减少，在导尿组和导尿加糖尿病组中增加。平滑肌和尿路上皮在导尿组和导尿加糖尿病组中减少。糖尿病和导尿加糖尿病大鼠的硝基酪氨酸和 Mn 超氧化物歧化酶增加。
多尿引起膀胱肥大，而高血糖引起膀胱中大量氧化应激，这可能在晚期糖尿病膀胱功能障碍中具有致病作用。
