Cucchi A
Divisione di Urologia, Policlinico S. Matteo, Pavia, Italy.
Br J Urol. 1992 Mar;69(3):272-6. doi: 10.1111/j.1464-410x.1992.tb15527.x.
Forty men with bladder outflow obstruction from benign prostatic hypertrophy were investigated urodynamically by medium-fill water cystometry and pressure flow study. The most obstructed patients proved to be unstable. A positive link was found between the degree of obstruction, as assessed by the opening pressure (i.e. the detrusor pressure needed to start micturition), and the maximum mechanical power generated by the contracting bladder during voiding. What seems most striking, is that neither detrusor contraction velocity nor the urine flow rate fully mirrored the degree of obstruction--i.e. the opening pressure and the maximum contraction speed did not show a negative correlation, but rather a weak (though insignificant) positive link, and the flow rate decreased only slightly (not significantly) when obstruction increased. Such a surprising observation could be explained by the fact that prostatic obstruction produces both collagen infiltration into the bladder muscle (this affecting the spread of the depolarisation wave) and, at the same time, denervation supersensitivity. The latter actually yields a decrease in electrical resistance between the detrusor smooth muscle cells (and thereby an enhanced synchronisation of the detrusor contraction), which might be only partly cancelled by the effects of collagenosis.
对40例因良性前列腺增生导致膀胱流出道梗阻的男性患者，采用中等量充盈膀胱测压法和压力流率研究进行尿动力学检查。梗阻最严重的患者被证明存在不稳定情况。通过起始压力（即开始排尿所需的逼尿肌压力）评估的梗阻程度与排尿期间收缩膀胱产生的最大机械功率之间发现了正相关关系。最引人注目的是，逼尿肌收缩速度和尿流率均未完全反映梗阻程度——即起始压力和最大收缩速度并非呈负相关，而是呈现出微弱（尽管不显著）的正相关，并且当梗阻增加时，尿流率仅略有下降（不显著）。这种令人惊讶的观察结果可以通过以下事实来解释：前列腺梗阻既会导致胶原蛋白浸润到膀胱肌肉中（这会影响去极化波的传播），同时也会引起去神经超敏反应。后者实际上会导致逼尿肌平滑肌细胞之间的电阻降低（从而增强逼尿肌收缩的同步性），而这种作用可能仅部分被胶原病的影响所抵消。
