Eika B, Levin R M, Longhurst P A
Division of Urology, University of Pennsylvania School of Medicine, Philadelphia.
J Urol. 1994 Feb;151(2):496-502. doi: 10.1016/s0022-5347(17)35001-2.
In vivo and in vitro bladder function were studied in three different models of increased diuresis: 1) Brattleboro rats with hereditary diabetes insipidus (di/di), 2) Sprague-Dawley rats with streptozotocin-induced diabetes mellitus (STZ), and 3) Sprague-Dawley rats with increased diuresis due to 5% sucrose added to the drinking water. When compared with controls, all three models showed bladder mass, increased water consumption and urine output, higher mean and maximal increased micturition volumes, and greater bladder capacity and compliance by in vitro cystometry. The changes were more extensive in di/di rats than in the STZ and sucrose-drinking rats. The concentration of bladder collagen decreased in all three rat models when compared with controls. However, the collagen concentration of STZ bladders was significantly lower than the collagen concentration of di/di and sucrose bladders, suggesting that the decrease in bladder collagen concentration associated with experimental diabetes mellitus is only partly related to the increased diuresis. Contractile function was studied using a whole bladder model. Responses of whole bladders from control and diabetic rats to electrical field stimulation, carbachol and KCl were identical. Volume-pressure relations of the isolated whole bladder showed that the magnitude of the contractile response to KCl is constant at intravesical volumes ranging from about 10 to 95% of cytometrical bladder capacity. Bladders from Brattleboro di/di rats and STZ rats showed a rightward shift of volume-passive pressure curves when compared with appropriate controls. Bladders from sucrose-drinking rats had volume-passive pressure curves similar to the bladders from controls. This study suggests that while contractile function remains intact with increased diuresis, the passive function changes, with the bladder becoming more distensible.
1)患有遗传性尿崩症(di/di)的布拉特洛维大鼠,2)链脲佐菌素诱导的糖尿病(STZ)的斯普拉格-道利大鼠,以及3)因饮用水中添加5%蔗糖而导致利尿增加的斯普拉格-道利大鼠。与对照组相比,所有三种模型均显示膀胱重量增加、饮水量和尿量增加、平均和最大排尿量增加,以及通过体外膀胱测压法测得的膀胱容量和顺应性增加。di/di大鼠的变化比STZ大鼠和饮用蔗糖水的大鼠更广泛。与对照组相比,所有三种大鼠模型的膀胱胶原蛋白浓度均降低。然而,STZ膀胱的胶原蛋白浓度明显低于di/di和蔗糖膀胱的胶原蛋白浓度,这表明与实验性糖尿病相关的膀胱胶原蛋白浓度降低仅部分与利尿增加有关。使用全膀胱模型研究收缩功能。对照组和糖尿病大鼠的全膀胱对电场刺激、卡巴胆碱和氯化钾的反应相同。分离的全膀胱的容积-压力关系表明,在膀胱内容积范围为膀胱测压容量的约10%至95%时,对氯化钾的收缩反应幅度恒定。与适当的对照组相比,布拉特洛维di/di大鼠和STZ大鼠的膀胱容积-被动压力曲线向右移位。饮用蔗糖水的大鼠的膀胱具有与对照组膀胱相似的容积-被动压力曲线。这项研究表明,虽然利尿增加时收缩功能保持完整,但被动功能发生变化,膀胱变得更具扩张性。