Azadzoi Kazem M, Siroky Mike B
VA Boston Healthcare System and Boston University School of Medicine.
J Biochem Pharmacol Res. 2013;1(1):64-74.
The etiology of lower urinary tract symptoms is poorly understood. The pathophysiology of detrusor instability, voiding dysfunction and pelvic pain in patients with non-obstructed bladder remains highly controversial. In the male, most cases of lower urinary tract symptoms are attributed to bladder outlet obstruction due to benign prostatic hyperplasia. However, urodynamic data have revealed that in approximately one third to more than one half of cases, lower urinary tract symptoms are not associated with enlarged prostate or bladder outlet obstruction. Interestingly, lower urinary tract symptoms questionnaires in women yield scores that are similar to their age-matched male counterparts. These observations imply that aging-associated sex-independent changes in bladder vasculature, nerves, smooth muscle and epithelium may play a role in the development of lower urinary tract symptoms. Epidemiologic studies have shown a close correlation between vascular occlusive disorders and the prevalence of lower urinary tract symptoms. International prostate symptom scores were found to be significantly worse in men with cardiovascular disorders than symptomatic patients without cardiovascular problems. Clinical trials have revealed a close correlation between decreased pelvic blood flow and severity of lower urinary tract symptoms in the elderly patients. Studies with experimental models of pelvic ischemia have shown that accumulation of reactive oxygen species in the ischemic bladder initiates a cascade of cellular, subcellular and molecular reactions. These reactions to ischemia appear to compromise bladder structure and function leading to neurodegeneration, smooth muscle instability, increased contractile activity, fibrosis and non-compliance. These observations collectively introduce a new concept in the pathophysiology of voiding dysfunction suggesting that pelvic ischemia may be an independent factor in the development of non-obstructed non-neurogenic overactive bladder and lower urinary tract symptoms.
下尿路症状的病因目前仍不太清楚。在膀胱无梗阻的患者中，逼尿肌不稳定、排尿功能障碍和盆腔疼痛的病理生理学仍存在很大争议。在男性中，大多数下尿路症状病例归因于良性前列腺增生导致的膀胱出口梗阻。然而，尿动力学数据显示，在大约三分之一至超过一半的病例中，下尿路症状与前列腺增大或膀胱出口梗阻无关。有趣的是，女性下尿路症状问卷得分与年龄匹配的男性相似。这些观察结果表明，与衰老相关的膀胱血管、神经、平滑肌和上皮的性别独立变化可能在下尿路症状的发生中起作用。流行病学研究表明，血管闭塞性疾病与下尿路症状的患病率密切相关。发现患有心血管疾病的男性的国际前列腺症状评分明显比没有心血管问题的有症状患者更差。临床试验表明，老年患者盆腔血流减少与下尿路症状严重程度密切相关。盆腔缺血实验模型研究表明，缺血膀胱中活性氧的积累引发了一系列细胞、亚细胞和分子反应。这些对缺血的反应似乎损害了膀胱结构和功能，导致神经退行性变、平滑肌不稳定、收缩活动增加、纤维化和顺应性降低。这些观察结果共同提出了排尿功能障碍病理生理学的一个新概念，表明盆腔缺血可能是无梗阻性非神经源性膀胱过度活动症和下尿路症状发生的一个独立因素。
