External urethral sphincter activity in diabetic rats

Abstract

To examine the temporal effects of diabetes on the bladder and the external urethral sphincter (EUS) activity in rats. Female Sprague-Dawley rats (n = 24) were divided into two groups: streptozotocin-induced diabetic rats and age-matched controls. Cystometrograms (CMGs) were taken under urethane anesthesia and electromyograms (EMG) of the EUS were evaluated in all rats at 6 and 20 weeks after diabetes induction. After EMG assessment, the tissues of the urethra were harvested for morphological examination. Diabetes caused reduction of body weight, but an increase in bladder weight. CMG measurements showed diabetes increased threshold volume, contraction duration, high-frequency oscillations (HFO), and residual volume. Peak contraction amplitude increased in 6-week but not 20-week diabetic rats. EUS-EMG measurements showed increased frequency of EUS-EMG bursting discharge during voiding in 6-week diabetic rats (8.1 +/- 0.2 vs. 6.9 +/- 0.6/sec) but not in 20-week (5.8 +/- 0.3 vs. 6.0 +/- 0.2/sec) diabetic rats compared with controls. EUS-EMG bursting periods were also increased in both 6-week and 20-week diabetic rats compared with controls. EUS-EMG silent periods were reduced in 6-week diabetic rats, but were not changed in 20-week diabetic rats compared with controls. Active periods did not change in 20-week diabetic rats, but increased in 6-week diabetic rats compared with controls. Morphometric analysis showed atrophy of the EUS after 20 week but not 6 weeks of DM induction. Our data indicates diabetes causes functional and anatomical abnormalities of the EUS. These abnormalities may contribute to the time-dependent bladder dysfunction in diabetic rats.