Prieto Chaparro L, Salinas Casado J, Barba Solana C, Resel Estévez L
Servicio de Urología, Hospital Virgen de los Lirios, Alcoy, Alicante, España.
Arch Esp Urol. 1996 Sep;49(7):727-39.
To analyze the urodynamic and ultrastructural characteristics of impaired detrusor contractility in patients with prostatism in comparison with lower urinary tract obstruction.
The study comprised 200 male patients (mean age 65.3 years) with prostatism submitted to a complete urodynamic study. An ultrastructural study was randomly performed in 40 patients and analyzed 600 detrusor muscle images to determine the smooth muscle cell and interstitial changes. Detrusor urodynamics were compared with the ultrastructural cell and interstitial changes of the bladder smooth muscle.
Urinary symptoms or free flowmetry alone failed to predict detrusor urodynamics. Urodynamic diagnosis was based on the detrusor pressure-flow study. We observed ultrastructural degenerative cell changes with statistical significance in impaired detrusor contractility such as no branching and intertwining of cells, absence of caveoles, perinuclear degeneration with vacuolization, destructured myofilament system with diminished anchorage plates and collagen infiltrating the interstitium with loss of bladder muscle fascicle organization.
Impaired detrusor contractility is a urodynamic diagnosis that should be taken into account in patients with prostatism. The diagnosis of this condition requires performing a pressure-flow study. Impaired detrusor contractility showed a morphological and ultrastructural correlation with degenerative changes of the bladder muscle.
比较前列腺增生症患者与下尿路梗阻患者逼尿肌收缩功能受损的尿动力学和超微结构特征。
该研究纳入了200例接受完整尿动力学检查的前列腺增生症男性患者(平均年龄65.3岁)。对其中40例患者进行随机超微结构研究,分析600张逼尿肌图像以确定平滑肌细胞和间质变化。将逼尿肌尿动力学与膀胱平滑肌的超微结构细胞和间质变化进行比较。
仅依据排尿症状或自由尿流率无法预测逼尿肌尿动力学。尿动力学诊断基于逼尿肌压力-流率研究。我们观察到在逼尿肌收缩功能受损时存在具有统计学意义的超微结构退行性细胞变化,如细胞无分支和交织、无小窝、核周变性伴空泡形成、肌丝系统结构破坏且锚定板减少以及胶原蛋白浸润间质导致膀胱肌束组织丧失。
逼尿肌收缩功能受损是一种尿动力学诊断,前列腺增生症患者应予以考虑。该病症的诊断需要进行压力-流率研究。逼尿肌收缩功能受损表现出与膀胱肌肉退行性变化的形态学和超微结构相关性。