New Model of BPH with Slowly Advancing Obstruction to Investigate Pathophysiology and Mechanism of Obstructed Bladder

缓慢推进梗阻的 BPH 新模型研究膀胱梗阻的病理生理学和机制

• 批准号: 20591884
• 负责人: YAMAGUCHI Osamu
• 金额: $ 3.08万
• 依托单位: Fukushima Medical University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2008
• 资助国家: 日本
• 起止时间: 2008 至 2010
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-20591884/
• 关键词: 前立腺肥大症; 尿流動態検査; 閉塞モデル; 増殖因子; 尿流動態検査医

In the present study, using beagle dogs, we created a new animal model of benign prostatic obstruction, in which prostate would occlude the bladder outlet as prostate grows. This model showed urinary frequency, an increase in detrusor pressure during voiding and a mild degree of residual volume, which resembles a micturition behavior of patients with benign prostatic hyperplasia (BPH). In the obstructed bladder of this new model, the expression of smooth muscle growth factor (HB-EGF) was higher than that of fibrous growth factor such as TGF-β1while smooth muscle cell apoptosis was suppressed. These results suggest that compensatory muscle hypertrophy or hyperplasia may serve to sustain the ability of detrusor to contract.

在本研究中，我们使用比格犬，建立了一种新的良性前列腺阻塞的动物模型，在该模型中，前列腺会随着前列腺的生长而阻塞膀胱出口。该模型显示排尿频率，排尿期间逼尿肌压力增加和轻度残余容量，这类似于良性前列腺增生（BPH）患者的排尿行为。在梗阻性膀胱中，平滑肌生长因子（HB-EGF）的表达高于纤维生长因子TGF-β 1，而平滑肌细胞凋亡受到抑制。这些结果表明，代偿性肌肉肥大或增生可能有助于维持逼尿肌的收缩能力。