CAJ | 학술논문

目的建造高位脊髓损伤所致神经源性膀胱的大鼠模型,研究神经源性膀胱排尿功能的变化及肾脏功能形态学的早期变化.方法 60只雌性Wistar大鼠随机分为模型组和对照组.模型组于T10处横断脊髓.对照组只在相同平面暴露脊髓.不做横断.分别在术后6、10、14周对2组大鼠行尿动力学检测;取尿液检测尿酶NAG水平及细菌培养、鉴定;取血测尿素氮;取.肾脏标本观察形态学变化.结果尿动力学检杳模型组大鼠在膀胱充盈期表现为逼尿肌反射亢进、逼尿肌漏尿点压力增高、顺应性初期增高后随着造模时间延长逐渐下降.模型组大鼠均存在泌尿系感染,尿酶NAG增高明显.大体标本未见明显输尿管增粗、肾积水.光镜下可见肾盂上皮有炎性浸润.肾小管出现损害,间质可见灶状分布的纤维化.肾小球未见明显异常.电镜下见肾小管上皮细胞肿胀.细胞器减少,肾小管刷状缘、线粒体嵴排列紊乱,基底膜基本完整.结论脊髓损伤后神经源性膀胱排尿功能发生明显异常,肾小管间质病变在评价肾功能损害上比肾小球病理改变更有意义.
목적 건조고위척수손상소치신경원성방광적대서모형,연구신경원성방광배뇨공능적변화급신장공능형태학적조기변화.방법 60지자성Wistar대서수궤분위모형조화대조조.모형조우T10처횡단척수.대조조지재상동평면폭로척수.불주횡단.분별재술후6、10、14주대2조대서행뇨동역학검측;취뇨액검측뇨매NAG수평급세균배양、감정;취혈측뇨소담;취.신장표본관찰형태학변화.결과 뇨동역학검묘모형조대서재방광충영기표현위핍뇨기반사항진、핍뇨기루뇨점압력증고、순응성초기증고후수착조모시간연장축점하강.모형조대서균존재비뇨계감염,뇨매NAG증고명현.대체표본미견명현수뇨관증조、신적수.광경하가견신우상피유염성침윤.신소관출현손해,간질가견조상분포적섬유화.신소구미견명현이상.전경하견신소관상피세포종창.세포기감소,신소관쇄상연、선립체척배렬문란,기저막기본완정.결론척수손상후신경원성방광배뇨공능발생명현이상,신소관간질병변재평개신공능손해상비신소구병리개변경유의의.
Objective To build the rat animal model of neurogenic bladder induced by spinal cord injury (SCI) and to nvestigate the changes of bladder and upper urinary tract function in this animal model. Methods A total of 60 female Wistar rats were randomly allocated into SCI group and sham group. Complete spinal cord transection was established by cutting out of dura at T10 in SCI group. The sham operation group was done only expose dura of T10 without transection. Urodynamic monitor was performed on rats at 6, 10 and 14 weeks. Urine was sent to do biochemistry examination, including NAG, bacteria count and culture. Blood was sent to detect BUN. Then put animals to death and take kidney specimens to do pathological examination. Results Urodynamic monitoring in rats revealed significant changes in the activity of the lower urinary tract after spinal cord transection. SCI rats exhibited detrusor hyperreflexia during bladder filling, higher leak point pressure, increased compliance at first and then decreased compliance compared with sham rats. All rats had urinary tract infection after the spinal cord injury. The level of NAG in SCI rats was increased. Hydroureterosis and hydronephrosis were not seen in SCI rats. Inflammatory infiltration in pelvis'epithelium and noticeable fibrous degeneration in interstitium were seen under light microscope, but glomcrulus was nearly normal. Under electron microscope, swelled epithelial cells, decreased organdie, and disorderly arrangement of renal tubule brush border and mitochondrial crista were noted. Conclusions Neurogenic bladder induced by spinal cord injury reveals significant changes in the activity of the lower urinary tract. Pathological changes of renal tubule and interstitium are more sensitive than glomcrulus in the evaluation of renal function.