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SUFU 2007 - External Urethral Sphincter Dysfunction in Diabetic Rats Show Comments PDF Print E-mail
  
Tuesday, 13 March 2007

Guiming Liu, Firouz Daneshgari.

The Cleveland Clinic Foundation, Cleveland, Ohio

Introduction and Objectives: Lower urinary tract complications are one of the most prevalent complications in diabetes mellitus (DM). We and others have demonstrated that the temporal course of diabetic bladder function in small animal models of DM include compensated and decompensated bladder function. However, little is known about the effects of DM on urethral function. The aim of this study was to examine the effects of DM duration (6 and 20 week after DM induction) on external urethral sphincter (EUS) activity and its contribution to the temporal course of voiding dysfunction seen in diabetic rats.

Methods: 36 Male SD rats were divided into 3 groups: streptozotocin-induced diabetics, 5% sucrose-induced diuretics, and age, sex-matched controls. Cystometry (CMG) under urethane anesthesia and EUS electromyogram (EMG) were evaluated in all rats after 6 and 20 week of disease induction. After EMG measurement, the mid-urethra were harvested for morphological examination.

Results: Diabetes caused reduction of body weight compared to diuresis and controls, and the bladders of diabetic and diuretic rats weighed more than the controls after 6- or 20-week induction. CMG measurements showed diabetes and diuresis increase bladder capacity, contraction duration and high-frequency oscillations (HFO). Peak contraction amplitude increased in 6-week but not in 20-week diabetic and diuretic rats. EUS-EMG measurements showed frequency of EUS-EMG bursting discharge during voiding was significantly increased in 6-week (8.1±0.2, 8.2±0.5, 6.9±0.6/sec, respectively) but not in 20-week (5.8±0.3, 6.3±0.4, 6.0±0.2/sec, respectively) diabetic and diuretic rats compare to controls. EUS-EMG bursting period increased in 6-week (6.8±0.3, 5.5±0.1, 4.1±0.6 sec, respectively) and 20-week (7.5±0.6, 6.5±0.6, 4.3±0.4 sec, respectively) diabetic and diuretic rats compare to controls. EUS-EMG silent periods were reduced in 6-week (0.073±0.003, 0.080±0.008, 0.096±0.012 sec, respectively) but not in 20-week (0.135±0.015, 0.120±0.007, 0.115±0.005 sec, respectively) diabetic and diuretic rats compare to controls. Morphometric analysis showed atrophy of striated muscle in the EUS after 20 week but not 6 week of DM induction.

Conclusions: This data indicate that the urethral relaxation mechanism during reflex bladder voiding in rat is impaired in DM rat. Diabetes causes EUS-EMG abnormalities and anatomical alterations of the EUS, which may partially contribute to the time-dependent voiding dysfunction in diabetic rats. Diabetes-associated diuresis accounts for a portion of these changes.

Source of Funding: Supported by grants NIH-NIDDK-DK02631; U01-DK61018; Young-Investigator award of the National Kidney Foundation; Grant-in aid by the Diabetic Association of the Greater Cleveland; and Juvenile Diabetes Research Foundation Fellowship (to G. Liu).

UroToday.com Coverage of SUFU 2007

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