Diabetic urethropathy compounds the effects of diabetic cystopathy.
Diabetic urethropathy compounds the effects of diabetic cystopathy.
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DOI：
10.1016/j.juro.2007.06.042
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发表时间：
2007-11
期刊：
影响因子：
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通讯作者：
Zhongguang Yang;P. C. Dolber;M. Fraser
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文献类型：
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作者：
Zhongguang Yang;P. C. Dolber;M. Fraser
目的观察短期和长期糖尿病对尿道功能的影响，探讨尿道功能障碍对糖尿病排尿功能障碍的影响。材料与方法用脲烷麻醉的雌性Sprague-Dawley大鼠（Charles River Laboratories, Wilmington, Massachusetts），在链脲霉素诱导糖尿病后5周和10周测量膀胱等容压、尿道灌注压和尿道外括约肌肌电图。观察糖尿病患者和年龄匹配对照组连续给予骨骼肌阻滞剂α-班加罗毒素、一氧化氮合酶抑制剂n ω-硝基- l -精氨酸和α-肾上腺素能激动剂l -苯肾上腺素的尿道反应。结果糖尿病大鼠膀胱压力和收缩幅度明显降低。约30%的糖尿病大鼠出现逼尿肌-括约肌协同障碍，而对照组从未出现过。α-Bungarotoxin引起糖尿病大鼠基线尿道灌注压比对照组下降更大（约40% vs约15%）。糖尿病大鼠膀胱收缩相关尿道平滑肌弛豫幅度明显小于对照组。ω-硝基- l -精氨酸对糖尿病大鼠尿道舒张无明显抑制作用。l -苯肾上腺素显著提高糖尿病大鼠的基线尿道灌注压，而对照组无显著升高。10周糖尿病大鼠对n -硝基- l -精氨酸不敏感和对l -苯肾上腺素过敏的非相关情况比对照组更常见。结论糖尿病性尿道病变以尿道外括约肌功能障碍、尿道平滑肌舒张和一氧化氮反应性降低、尿道平滑肌对α - 1肾上腺素能激动剂的反应性升高为特征。这些变化增加了出口阻力，从而降低了排尿效率。这加剧了排尿功能障碍，造成了下尿路损伤和功能障碍的恶性循环。可能需要针对出口阻力进行早期干预。
PurposeThe effects of short-term and long-term diabetes mellitus on urethral function were investigated to determine the contribution of urethral dysfunction to diabetes mellitus voiding dysfunction.Materials and MethodsIsovolumetric bladder pressure, urethral perfusion pressure and external urethral sphincter electromyography were measured in urethane anesthetized, female Sprague-Dawley rats (Charles River Laboratories, Wilmington, Massachusetts) 5 or 10 weeks after streptozotocin induced diabetes mellitus. Urethral responses to serial administration of the skeletal muscle blocker α-bungarotoxin, the nitric oxide synthase inhibitor Nω-nitro-L-arginine and the α-adrenergic agonist L-phenylephrine were determined in diabetes mellitus and age matched controls.ResultsPeak bladder pressures and contraction amplitudes were significantly decreased in diabetes mellitus rats. Detrusor-sphincter dyssynergia occurred in approximately 30% of diabetes mellitus rats but never in controls. α-Bungarotoxin caused a greater decrease in baseline urethral perfusion pressure in diabetes mellitus rats than in controls (approximately 40% vs approximately 15%). Bladder contraction associated urethral smooth muscle relaxation amplitudes were significantly less in diabetes mellitus rats than in controls. Nω-nitro-L-arginine significantly suppressed urethral relaxation in controls but not in diabetes mellitus rats. L-phenylephrine significantly increased baseline urethral perfusion pressure in diabetes mellitus rats but not in controls. The unassociated conditions of insensitivity to N-nitro-L-arginine and hypersensitivity to L-phenylephrine were more common in 10-week diabetes mellitus rats than in control rats.ConclusionsDiabetes mellitus induced urethropathy is characterized by external urethral sphincter dysfunction, decreased urethral smooth muscle relaxation and nitric oxide responsiveness, and increased urethral smooth muscle responsiveness to α1-adrenergic agonists. These changes increase outlet resistance and, thereby, decrease voiding efficiency. This exacerbates voiding dysfunction, creating a vicious cycle of progressive lower urinary tract damage and dysfunction. Early intervention targeting outlet resistance may be indicated.