CAJ | 학술논문

背景:近几年来有文献报道脑死亡供体器官损伤以及移植之后移植物质量下降,与机体非特异性炎症反应有关.目的:建立兔脑死亡模型,观察脑死亡后不同时间点肾脏形态学及功能学方面的变化情况,并揭示其可能的作用机制,为临床合理利用脑死亡供体进行肾脏移植提供实验依据.方法:采用兔缓慢颅内加压法建立脑死亡模型.30只大鼠随机数字表法分为3组,正常组(n=5):仅作持续麻醉维持,不予处理;对照组(n=5):麻醉后进行开关腹手术并钻孔开颅;实验组(n=20):麻醉后建立脑死亡模型.在确定脑死亡后,分别观察2,4,6,8 h 后肾脏各指标变化.结果与结论:随着脑死亡时间的延长,血清中尿素氮、肌酐的浓度不断增加,白细胞介素1β,6,8、肿瘤坏死因子α的水平也不断升高;苏木精-伊红染色和原位末端凋亡法结果显示,随着脑死亡时间的延长,肾脏损伤程度有所增加、肾脏组织中 PKCα mRNA、蛋白质的表达趋势亦如此.说明脑死亡状态可以导致肾脏形态学及功能学方面的改变,且随着时间的延长而逐渐加重,该现象可能与 PKCα的激活、炎症递质的释放有关.
배경:근궤년래유문헌보도뇌사망공체기관손상이급이식지후이식물질량하강,여궤체비특이성염증반응유관.목적:건립토뇌사망모형,관찰뇌사망후불동시간점신장형태학급공능학방면적변화정황,병게시기가능적작용궤제,위림상합리이용뇌사망공체진행신장이식제공실험의거.방법:채용토완만로내가압법건립뇌사망모형.30지대서수궤수자표법분위3조,정상조(n=5):부작지속마취유지,불여처리;대조조(n=5):마취후진행개관복수술병찬공개로;실험조(n=20):마취후건립뇌사망모형.재학정뇌사망후,분별관찰2,4,6,8 h 후신장각지표변화.결과여결론:수착뇌사망시간적연장,혈청중뇨소담、기항적농도불단증가,백세포개소1β,6,8、종류배사인자α적수평야불단승고;소목정-이홍염색화원위말단조망법결과현시,수착뇌사망시간적연장,신장손상정도유소증가、신장조직중 PKCα mRNA、단백질적표체추세역여차.설명뇌사망상태가이도치신장형태학급공능학방면적개변,차수착시간적연장이축점가중,해현상가능여 PKCα적격활、염증체질적석방유관.
BACKGROUND: Recent studies have reported that brain-dead donor organ injury and decreased graft quality after transplantation was related with non-specific inflammatory response. OBJECTIVE: To establish the rabbit brain death model, and to observe the change of kidney function and morphology in the rabbits at different time points after brain death and explore its possible mechanism, which provide experimental evidence for the clinical use of kidney transplant with brain-dead donor. METHODS: Slow intracranial pressure method was used to establish rabbit brain death model. Thirty healthy rabbits were divided into three groups. Normal group (n=5): maintained with continuous anesthesia and without any processed. Control group (n=5): abdominal surgery and dril craniotomy were performed after anesthesia. Experimental group (n=5):brain death model was established after anesthesia. The change of each indicator of the kidney was observed at 2, 4, 6 and 8 hours after brain death. RESULTS AND CONCLUSION: With the extension of time of brain death, the level of serum blood urea nitrogen, creatinine and interleukin-1β, interleukin-6, interleukin-8 and tumor necrosis factor α was increased gradual y. Results of hematoxylin-eosin staining and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay showed that with the extension of brain death time, the extent of kidney injury was increased, as wel as the expression of PKCα mRNA and the protein in kidney tissues. These results show that brain death state can lead to the change of kidney morphology and function in a time-dependent manner, and this phenomenon may be related with the activation of PKCα and release of inflammatory mediators.