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目的观察2型糖尿病大鼠膀胱逼尿肌超微改变,从细胞形态学分析糖尿病膀胱功能障碍发病机理。方法建立STZ诱导糖尿病大鼠模型,在4、12周时电镜下观察膀胱逼尿肌超微结构。结果电镜下逼尿肌表现为逼尿肌细胞体积增大,SMC之间的间隙缩小,细胞间胶原纤维增多,细胞间中间连接减少,胞突连接及缝隙连接多见。12周时上述改变较4周明显加重。与时间有明显相关性,此损害过程为一个神经纤维束减少、膀胱逼尿肌代偿与重建,最后导致膀胱功能障碍的过程。结论糖尿病早期,大鼠膀胱逼尿肌的平滑肌、细胞间质和神经纤维均有改变,随着时间的延长变明显。形态学方面的检测为神经电生理检查和尿动力学提供佐证,为临床诊断治疗糖尿病膀胱病提供依据。
Objective To observe the ultrastructural changes of bladder detrusor in type 2 diabetic rats and to analyze the pathogenesis of diabetic bladder dysfunction by cell morphology. Methods STZ-induced diabetic rat models were established. The ultrastructure of bladder detrusor muscle was observed under the electron microscope at 4 and 12 weeks. Results Detrusor muscle showed detrusor muscle volume increased under electron microscope, the gap between SMCs was narrowed, the number of intercellular collagen fibers increased, and the number of intercellular junctions decreased. Cell junction and gap junction were more common. The above changes were significantly worse than those at 4 weeks at 12 weeks. And time have obvious relevance, this damage process is a decrease of a nerve fiber bundle, bladder detrusor compensation and reconstruction, and finally lead to bladder dysfunction. Conclusion In the early stage of diabetes, the smooth muscle, interstitial cells and nerve fibers in the detrusor of rats have changed, and become obvious with the extension of time. Morphological detection of neuroendocrine electrophysiology and urodynamics provide evidence for the clinical diagnosis and treatment of diabetic bladder disease provide the basis.