前列腺增生继发逼尿肌活动障碍的超微病理研究

Ultrastructural changes of detrusor dysfunction secondary to BPH

目的探讨前列腺增生(BPH)继发逼尿肌活动障碍的超微结构变化。方法以尿动力学检查为依据,在BPH患者中筛选出13例膀胱出口梗阻(BOO)者,分为逼尿肌不稳定(DI)组3例、逼尿肌收缩力低下(DH)组4例、逼尿肌无收缩(DA)组3例和逼尿肌正常收缩(DC)组3例,分别行透射电镜观察。结果 (1)逼尿肌不稳定组:逼尿肌平滑肌细胞(SMC)之间的间隙明显增宽,细胞间中间连接(IJ)明显减少,为缝隙连接和胞突连接所取代;(2)逼尿肌收缩力低下组:SMC形态大小不一,分布不均,肌丝紊乱,增宽的间隙中沉积大量胶原纤维;(3)逼尿肌无收缩组:SMC扭曲变形,胞浆中肌丝排列走行紊乱,致密体分布不均,线粒体减少,肌质膜下小凹(CV)减少。结论尿动力学表现不同的BPH继发逼尿肌活动障碍患者具有相应的逼尿肌超微结构病理改变,对BPH继发逼尿肌活动障碍的分类和治疗具有一定的价值。

Objective To investigate the ultrastructural changes of detrusor scecondary to benign prostatic hyperplasia（BPH）. Methods Based on the urodynamics results of 13 cases of bladder outlet obstruction（BOO） secondary to BPH, patients in our study were diagnosed and divided into three case groups： detrusor instability（DI） group（3 cases）, detrusor hypo-contractility（DH） group（4 cases）, detrusor acontractile（DA） group（3 cases） and a control group（3 cases） with normal detrusor contractility（DC）.Transmission electron microscopy（TEM） was used to examine the ultrastructure of detrusor. Results According to the results of TEM, some ultrastructural changes were observed in each group：（1） In DI group：a wide separation between detrusor smooth muscle cell（SMC） was observed in DI group with reduction of intermediate junction（IJ） and increased gap junction and cytoplasmic process junction;（2） In DH group：various sizes and shapes of SMC with malalignment of myofilament were observed. Abundant of collagen fibrils fulfill the expended intercellular space.（3） In DA group： different ultrastructure compared to that in NC group were observed： maldistribution of SMC with distorted contour, malalignment and atrophy of myofilament, maldistribution of dense body and reduction of caveali（CV） and chondriosome in the SMC.Conclusions Different ultrastructure of detrusor were observed in BPH patient with different urodynamics results. These results may be valuable in the classification and treatment for patients with detrusor dysfunction secondary to BPH.