AIM: To examine the temporal effects of diabetes on the bladder and the external urethral sphincter (EUS) activity in rats. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
AIM: To examine the temporal effects of diabetes on the bladder and the external urethral sphincter (EUS) activity in rats. METHODS: Female Sprague-Dawley rats (n = 24) were divided into two groups: streptozotocin-induced diabeticrats 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. RESULTS: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 diabeticrats. EUS-EMG measurements showed increased frequency of EUS-EMG bursting discharge during voiding in 6-week diabeticrats (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) diabeticrats compared with controls. EUS-EMG bursting periods were also increased in both 6-week and 20-week diabeticrats compared with controls. EUS-EMG silent periods were reduced in 6-week diabeticrats, but were not changed in 20-week diabeticrats compared with controls. Active periods did not change in 20-week diabeticrats, but increased in 6-week diabeticrats compared with controls. Morphometric analysis showed atrophy of the EUS after 20 week but not 6 weeks of DM induction. CONCLUSIONS: Our data indicates diabetes causes functional and anatomical abnormalities of the EUS. These abnormalities may contribute to the time-dependent bladder dysfunction in diabeticrats.
Authors: Hui Q Pan; Dan L Lin; Christopher Strauch; Robert S Butler; Vincent M Monnier; Firouz Daneshgari; Margot S Damaser Journal: Am J Physiol Renal Physiol Date: 2010-09-29