Steers W D, Mackway A M, Ciambotti J, de Groat W C
Department of Pharmacology, University of Pittsburgh, School of Medicine, Pennsylvania.
J Urol. 1990 May;143(5):1032-6. doi: 10.1016/s0022-5347(17)40177-7.
Streptozotocin-induced (STZ, 60 mg./kg. I.V.) diabetic male rats underwent cystometrographic (CMG) and electrophysiologic evaluations under urethane anesthesia (1.2 gm./kg.) to determine whether the neural pathways to the urinary bladder are altered in these animals. Diabetic rats (n = 6) in comparison to controls (n = 8) had significantly greater micturition volumes (3.0 +/- 0.8 ml. vs. 0.7 +/- 0.4 ml., p less than 0.001), bladder compliances (0.51 +/- 0.15 cm. H2O/ml. vs. 0.12 +/- 0.09 cm. H2O/ml., p less than 0.001) and bladder weights (225.2 +/- 21.4 mg. vs. 112.2 +/- 18.0 mg., p less than 0.01). No differences were noted in: 1) the thresholds or conduction velocities of axons in the bladder postganglionic nerves, 2) transmission in the major ganglion or 3) the latencies for firing in the supraspinal parasympathetic reflex pathway to the bladder. However, the supraspinal reflex, which was facilitated by bladder distension in 38% of control rats, was not facilitated in any diabetic rats. Another apparent difference in diabetic rats was the absence of spinal reflex response which was noted in 38% of control animals. This study confirmed that CMG changes in STZ-induced diabetic rats are similar to those observed clinically in patients with diabetic autonomic neuropathy, and in addition raise the possibility that these changes are produced by a defect in autonomic reflexes. It is also clear that alterations of the micturition reflex pathway in diabetic rats are distinct from those associated with another type of enlarged, abnormal bladder induced by bladder outlet obstruction.
用链脲佐菌素（STZ，静脉注射60毫克/千克）诱导的糖尿病雄性大鼠在氨基甲酸乙酯麻醉（1.2克/千克）下进行膀胱压力容积测定（CMG）和电生理评估，以确定这些动物中通往膀胱的神经通路是否改变。与对照组（n = 8）相比，糖尿病大鼠（n = 6）的排尿量显著更大（3.0±0.8毫升对0.7±0.4毫升，p<0.001），膀胱顺应性更高（0.51±0.15厘米水柱/毫升对0.12±0.09厘米水柱/毫升，p<0.001），膀胱重量更重（225.2±21.4毫克对112.2±18.0毫克，p<0.01）。在以下方面未观察到差异：1）膀胱节后神经中轴突的阈值或传导速度，2）主要神经节中的传递，或3）脊髓上副交感神经反射通路中膀胱放电的潜伏期。然而，在38%的对照大鼠中由膀胱扩张促进的脊髓上反射，在任何糖尿病大鼠中均未得到促进。糖尿病大鼠的另一个明显差异是在38%的对照动物中观察到的脊髓反射反应缺失。本研究证实，STZ诱导的糖尿病大鼠中的CMG变化与糖尿病自主神经病变患者临床观察到的变化相似，此外还增加了这些变化是由自主反射缺陷产生的可能性。同样清楚的是，糖尿病大鼠排尿反射通路的改变与由膀胱出口梗阻引起的另一种类型的扩大、异常膀胱相关的改变不同。
