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作 者:王军[1] 梁颖[2] 庄仕华[3] 李彤[1] 宋波[4] 金锡御[4] 叶章群[5]
机构地区:[1]武警新疆总队医院泌尿外科,新疆乌鲁木齐830000 [2]新疆医科大学公共卫生学院营养与食品卫生教研室,新疆乌鲁木齐830054 [3]武警新疆总队医院肝胆外科,新疆乌鲁木齐830000 [4]第三军医大学西南医院全军泌尿外科研究所,重庆400038 [5]华中科技大学同济医学院附属同济医院泌尿外科,湖北武汉430030
出 处:《新疆医科大学学报》2007年第8期803-806,共4页Journal of Xinjiang Medical University
摘 要:目的:探讨膀胱梗阻大鼠逼尿肌不稳定(detrusor instability,DI)与三磷酸肌醇[inositol(1,4,5)-trisphosphat,IP3]含量变化的关系。方法:建立DI大鼠模型,分别检测DI大鼠、逼尿肌稳定(detrusor stability,DS)大鼠及经卡巴可(Carbachol)处理的DS大鼠逼尿肌原代培养细胞IP3含量。结果:DI大鼠逼尿肌原代培养细胞IP3含量显著高于DS大鼠(P<0.01),经10-5mmol/L卡巴可刺激后,DS大鼠逼尿肌原代培养细胞IP3含量较刺激前显著升高(P<0.01)。结论:肌醇脂质信号传导通路可能参与了逼尿肌不稳定的形成,IP3含量的升高可能在其中起着重要作用。Objective: To investigate the relationship between detrusor instability secondary to bladder outlet obstruction and the content change of inositol (1,4,5)-trisphosphate (IP3) in rats. Methods: To set up the model of detrusor instability (DI) of rats, IP3 contents of detrusor cultured cell in DI rats, detrusor stability (DS) rats which stimulated by 10^-5M carbachol in DS rats were detected. Results: IPa contents of detrusor cultured cell of DI rats were significantly higher than those of DS rats (P 〈0.01), IP3 contents of DS rats detrusor cultured cell stimulated by 10-SM carbachol were also obviously higher than those of DS rats no stimulated (P d0.01). Conclusions: Inositol-lipid signal transduction pathway might participate the pathogenesis of DI and the increasing of IP3 contents might play a important role .
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