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机构地区:[1]嘉兴市第一医院泌尿外科,浙江嘉兴314001
出 处:《临床泌尿外科杂志》2008年第2期143-145,共3页Journal of Clinical Urology
摘 要:目的:探讨糖尿病(DM)对膀胱逼尿肌兴奋性、收缩性、顺应性的影响及糖尿病神经源性膀胱尿道功能障碍(NVUDD)的发病机制。方法:建立SD大鼠DM动物模型,于10周后行充盈性膀胱测压及离体逼尿肌条机械牵拉、电及胆碱类药物刺激试验。结果:DM动物模型10周后不稳定膀胱(DI)的发生率为64.7%,逼尿肌顺应性升高;DI组、DM后稳定组与正常对照组相比,牵拉逼尿肌致其出现收缩时的张力明显降低,电刺激产生的收缩力明显减弱;DI组逼尿肌胆碱类药物产生的收缩力明显减弱。结论:DM后NVUDD的发生率较高,其逼尿肌的收缩功能受损较重,DNBUD的发生与逼尿肌自身的神经源及肌源性改变密切相关。Objective:To study the influence of diabetes mellitus (DM) on detrusor excitability, contractility and compliance in order to elucidate the pathogenesis of neuropathic vesicourethal dysfunction of diabetic (NVUDD). Methods: Animal models of DM were made in SD rats 10 weeks later, the change of detrusor excitability, contractility and compliance were examined by means of cystometry and the in vitro detrusor strip study. Results:The rate of DI occurrence was 64.7% in the 10 weeks diabetic rats. The detrusor compliance increased significantly after (P〈0. 05). In DI group, the detrusor contraction took place with lower tension than the control and the stability group (P〈0.05). Conclusions:There is a higher occurrence rate of NVUDD after DM, and DI indicates impaired detrusor contraction. The mechanism of DI is closely related to the detrusor myogenic changes and the neuropathologic factor.
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