氯胺酮相关性膀胱炎致病机制的研究  

Pathogenesis of ketamine-associated cystitis model

作　　者：易小春[1] 吴天鹏[1] 刘凌琪[1] 段启新[1] 

机构地区：[1]武汉大学人民医院泌尿外科,430060

出　　处：《中华实验外科杂志》2013年第12期2528-2530,I0001,I0002,共5页Chinese Journal of Experimental Surgery

摘　　要：目的 建立氯胺酮相关性膀胱炎的动物模型,探讨其致病机制.方法 60只6～8周龄的C57小鼠分为实验组和对照组,两组分别按时间梯度再分为4、8、12周亚组,每组各10只.实验组给予氯胺酮100 mg/（kg·d）腹腔注射,对照组给予等量的生理盐水腹腔注射;分别于4、8、12周置于垫滤纸的方格中,观察每只小鼠的2h排尿次数,随后置于小鼠代谢笼中,收集24h尿液,检测尿中钾、钠离子及肌酐浓度;处死小鼠,取膀胱组织,行苏木素-伊红（HE）染色,光学显微镜观察形态学改变.结果 从8周起,实验组小鼠排尿次数增多,尿液中钾离子浓度降低,膀胱黏膜大量淋巴细胞浸润,部分膀胱组织可见鳞状细胞化生.结论 长期吸食氯胺酮可引起膀胱组织慢性炎症改变及上皮细胞鳞状化生,其损害机制可能与上皮屏障通透性改变有关.Objective To create a ketamine-associated cystitis model and preliminarily investigate the pathogenesis.Methods Sixty 6-8-week old female C57BL/6 mice were randomly divided into experimental group and control group,and subdivided into 4-,8-,and 12-week subgroups according to the time gradient,with 10 rats in each group.Ketamine,100 mg/kg,was intraperitoneally injected daily in experimental group,and normal saline was given in control group.During 2 h the number of micturitions was recorded,then the mice were placed in metabolic cages and 24-h urine was collected at 4th,8th and 12th week.Urinary potassium （K）,sodium （Na） and creatinine （Cr） were determined in 24-h urine samples.The bladders were harvested and subjected to HE staining,and histopathological changes were observed by light microscope.Results Increased frequency of micturitions and decreased urine potassium concentrations were noted in the experimental groups from the 8th week.Microscopy revealed submucosal congestion and mononuclear cell infiltration from 8th week and squqmous cell atypia was observed in the some samples.Conclusion Long-term ketamine abuse may lead to chronic inflammation of bladder tissue and epithelial squamous metaplasia,which might be related to the changes of epithelial barrier permeability.

关 键 词：氯胺酮 膀胱炎 尿钾 上皮屏障 模型 动物 

分 类 号：R694.3[医药卫生—泌尿科学]