Effects of streptozotocin-induced diabetes on bladder function in the rat.

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.