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초록

Introduction: Previous investigations on bladder innervation and function led to the conclusion that voiding dysfunction in the diabetic patient is resulted from autonomic and sensory neuropathy in bladder only. Materials and Methods: Total, 57 male Sprague-Dawley rats(29 diabetic and 28 control; 200-500g in weights), were included in this study. Diabetes was induced using Weir's method(neonatal streptozotocin injection method; 90 mg/kg) on the second day after birth, To evaluate the urethral resistance, the urodynamic study was performed using the two-channel BIOPAC system, double lumen catheter(16/20/22 G) through bladder dome, PE 10 catheter in the urethra. The detrusor pressure on urethral leaking(detrusor leak point pressure(LPP)) was compared in diabetic and control rats. Results: The DM models were compatible to the finding of NIDDM. On the urodynamic study, the detrusor LPPs of diabetic rats were significantly higher than those of control rats at the age of 12 and 24 weeks. On 36 weeks those were similar between DM and control rats. After intravenous injection of L-NAME, detrusor LPPs of diabetes were not changed while they were significantly increased in controls. After intravenous injection of SNP, detrusor LPPs were decreased in both diabetics and controls. Urethral immunohistochemistry showed that the number and immuno-reactivities of nNOS containing nerve fibers in diabetics were significantly decreased, compared to those in controls. Those findings were also prominent in older age within the group of both diabetics and controls. Conclusion: The results indicate that urethral resistance is gradually increased along with the duration of diabetes, which might be resulted from reduction of urethral NOS containing nerve. Urethral factor in DM cystopathy has an important role on the pathogenesis of voiding dysfunction in patients with diabetes.