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目的 为进一步阐明糖尿病膀胱病变的发病机理提供实验依据。 方法 以糖尿病大鼠为模型 ,蔗糖利尿鼠及正常大鼠为对照 ,作离体膀胱灌注测压观察膀胱顺应性改变 ;分别采用全膀胱及逼尿肌条对比研究膀胱舒缩功能变化。 结果 糖尿病组大鼠膀胱逼尿肌收缩力明显低于蔗糖利尿组及对照组 [分别为 (2 0 80± 6 38)、(31 6 6± 6 17)、(4 0 10± 7 2 1)g/ 10 0mgT];膀胱舒张功能显著下降 ,膀胱顺应性升高。 结论 糖尿病大鼠模型 12周时膀胱收缩、舒张功能明显受损 ,同时 ,膀胱顺应性异常也是致病机理之一 ;利尿 (多尿 )不是糖尿病膀胱病变的主要因素。
Objective To provide experimental evidence for further clarifying the pathogenesis of diabetic bladder disease. Methods Diabetic rats were used as the model, sucrose diuretic rats and normal rats as controls. The changes of bladder compliance were observed under the conditions of exsangial bladder perfusion pressure measurement. The changes of bladder systolic and diastolic function were compared using total bladder and detrusor strips respectively. Results Contractility of bladder detrusor muscle of diabetic rats was significantly lower than that of sucrose diuresis and control rats [(20 80 ± 6 38), (31 6 6 ± 6 17), (4 0 10 ± 7 2 1) g / 10 0mgT]; bladder diastolic function decreased significantly, bladder compliance increased. Conclusions The bladder contraction and diastolic function were significantly impaired in diabetic rats at 12 weeks. At the same time, abnormal bladder response was also one of the pathogenic mechanisms. Diuretic (polyuria) was not the main factor of diabetic bladder lesions.