膀胱出口梗阻后逼尿肌收缩功能异常机制的研究

Study of mechanism of dysfunction in detrusor muscle in patients after bladder outlet obstruction

目的探讨人膀胱出口梗阻(bladder outlet obstruction,BOO)后逼尿肌在收缩力、形态学以及酶学上的变化及意义。方法采集前列腺增生症患者和无BOO者各20例膀胱逼尿肌作为研究对象,测定收缩力、电镜观察超微结构以及用荧光分光度计分别对MDA含量和SOD、NOS、Ca2+Mg2+ATP酶的活力进行测定。结果BOO组逼尿肌收缩力(0.347±0.107)g明显低于对照组(0.598±0.167)g。BOO组逼尿肌中检测到的SOD(13.908±1.430)U/mg protein、NOS(1.274±0.137)U/mg protein以及Ca2+Mg2+ATP酶(0.903±0.266)μmol Pi/mg protein活力明显低于对照组逼尿肌的检测值(21.444±1.657)U/mg protein、(1.871±0.240)U/mg protein、(1.523±0.329)μmol Pi/mg protein,BOO组逼尿肌中检测到的MDA含量(2.488±0.383)nmol/mg protein要高于对照组中的检测值(1.872±0.170)nmol/mg protein。电镜观察到BOO组逼尿肌:平滑肌细胞(SMC)扭曲变形,肌丝走行紊乱,密体、密斑数量明显减少;肌细胞内出现大量溶酶体;SMC内线粒体空泡变性或絮状变性,粗面内质网脱颗粒;细胞核固缩,核膜表面呈锯齿状,核内高密度染色质凝聚堆积,已出现细胞调亡改变。结论缺血再灌注损伤参与人逼尿肌功能失代偿的演化过程,以致逼尿肌肌细胞超微结构出现衰亡的改变,收缩力受损,收缩能力减弱,这为保护BOO后逼尿肌收缩功能提供了新思路。

Objective To investigate the significance of contractility, morphologic and enzymatic changes of the detrusor muscle after bladder outlet obstruction （BOO）. Methods The bladder derusor muscles of 20 Benign prostatu Hyperplasia （BPH） patients with BOO （BOO group） and 20 patients of bladder tumor without BOO （control group） were collected. The contractility of detusor muscles was tested. Morphologic changes were observed under electron microscope. The MDA concentration and the activity of SOD, NOS and Ca^2＋ Mg^2＋-ATPase were measured. Results The detrusor muscle contractility（0. 347 ±0. 107） g, activity of SOD（ 13. 908 ±1. 430） U/rag protein, NOS（ 1. 274 ±0. 137） U/rag protein and Ca^2＋ Mg^2＋ -ATPase （0. 903±0. 266） μmol Pi/mg protein in BOO group was significantly lower than that in control group. In contrast, the concentration of MDA in BOO patients（2. 488 ±0. 383） nmol/mg protein was much higher than that in normal controls. Electron microscope results showed that smooth muscle cells （SMC） were twisted, in malalignment and some were dissolved. The dense body and dense patch were decreased. Lots of cytolysosomes were seen in the SMC. Mitochondria appeared vacuolar andfloccose degeneration and degranulation were seen in rough endoplasmic reticulum. The nucleus showed karyopycnotic, with nucleolemma serratus, and chromatin agglutinated. Conclusion It is supposed that ischemia-reperfusion injury may play a role in the dysfunctional progression of detrusor muscle in BOO patients. The detrusor muscle cells of BOO are in state of apoptosis. The contractility of detrusor muscle is damaged badly in BOO. It provides a new idea to protect the contractility of detrusor muscle in BOO patients.