Kudlacz E M, Chun A L, Skau K A, Gerald M C, Wallace L J
Division of Pharmacology, College of Pharmacy, Ohio State University, Columbus 43210.
Diabetes. 1988 Jul;37(7):949-55. doi: 10.2337/diab.37.7.949.
Studies were done to characterize the bladder dysfunction associated with diabetes mellitus and to distinguish between changes occurring from increased diuresis and autonomic neuropathy. Four experimental conditions were compared: control, 4-wk-streptozocin-induced diabetes, sucrose feeding (diuretic), and galactose feeding (diuretic and sugar alcohol). A 10-fold increase in urine output and 25-50% increases in bladder weight, protein content, and DNA content were observed in all noncontrol treatment groups. Compliance properties were studied by measuring the intravesicular pressure as the bladder was infused with buffer in vitro. All treated bladders exhibited a reduction in plateau pressure and an increase in fluid capacity. Thus, diuresis results in an increased bladder size, which correlates with an alteration of compliance properties. Nervous system control in anesthetized rats was examined by monitoring contractions as the bladder was infused with buffer. Three distinct patterns of response were observed: normal, diabetic, and diuretic (galactose and sucrose treatments). The difference between responses in diuretic and diabetic animals suggests the presence of a diabetes-induced alteration in nerve regulation of the bladder. Reserpine pretreatment of control or diuretic models produced marked changes in the pattern of contractions, whereas pretreatment of diabetic rats had only modest effects. This suggests that diabetic bladders were lacking sympathetic control before the drug treatment. When rats treated for 4 wk with galactose were removed from this diet for 4 wk before testing, the bladders responded similarly to controls. This observation, coupled with the fact that galactose did not produce the same response as diabetes in the in vivo experiment, suggests that the galactose model does not produce irreversible functional neuropathies.
开展了多项研究，以描述与糖尿病相关的膀胱功能障碍，并区分因多尿和自主神经病变引起的变化。比较了四种实验条件：对照、4周链脲佐菌素诱导的糖尿病、蔗糖喂养（利尿）和半乳糖喂养（利尿及糖醇）。在所有非对照治疗组中，尿量增加了10倍，膀胱重量、蛋白质含量和DNA含量增加了25 - 50%。通过在体外向膀胱灌注缓冲液时测量膀胱内压来研究顺应性特性。所有处理过的膀胱均表现出平台压降低和容量增加。因此，多尿导致膀胱体积增大，这与顺应性特性的改变相关。通过监测向膀胱灌注缓冲液时的收缩情况，研究了麻醉大鼠的神经系统控制。观察到三种不同的反应模式：正常、糖尿病和利尿（半乳糖和蔗糖处理）。利尿和糖尿病动物反应的差异表明，糖尿病会导致膀胱神经调节发生改变。对对照或利尿模型进行利血平预处理会使收缩模式产生显著变化，而对糖尿病大鼠进行预处理则只有适度影响。这表明在药物治疗前，糖尿病膀胱缺乏交感神经控制。当用半乳糖处理4周的大鼠在测试前4周停止该饮食时，膀胱的反应与对照相似。这一观察结果，再加上半乳糖在体内实验中未产生与糖尿病相同反应这一事实，表明半乳糖模型不会产生不可逆的功能性神经病变。
