中国组织工程研究

中国组织工程研究 ›› 2012, Vol. 16 ›› Issue (53): 10021-10026.doi: 10.3969/j.issn.2095-4344.2012.53.027

• 器官移植基础实验 basic experiments of organ transplantation • 上一篇    下一篇

兔脑死亡状态对肾脏损伤的影响机制

王甲甲，李 玲，钟自彪，范晓礼，乔兵兵，叶啟发   

  1. 武汉大学中南医院肝胆疾病研究院，湖北省武汉市 430071
  • 收稿日期:2012-03-16 修回日期:2012-04-25 出版日期:2012-12-30 发布日期:2012-12-30
  • 通讯作者: 叶啟发，博士，主任医师，武汉大学中南医院肝胆疾病研究院，湖北省武汉市 430071 yqf_china@163.com
  • 作者简介:王甲甲☆，女，1984年生，河南省三门峡市人，汉族，中南大学在读博士，主治医师，主要从事器官移植免疫方面的研究。 xywjj08@163.com

Mechanism of kidney injury in brain death rabbits

Wang Jia-jia, Li Ling, Zhong Zi-biao, Fan Xiao-li, Qiao Bing-bing, Ye Qi-fa   

  1. Institution of Hepatobiliary Disease, Zhongnan Hospital of Wuhan University, Wuhan 430071, Hubei Province, China
  • Received:2012-03-16 Revised:2012-04-25 Online:2012-12-30 Published:2012-12-30
  • Contact: Ye Qi-fa, Doctor, Chief physician, Institution of Hepatobiliary Disease, Zhongnan Hospital of Wuhan University, Wuhan 430071, Hubei Province, China yqf_china@163.com
  • About author:Wang Jia-jia☆, Studying for doctorate, Attending physician, Institution of Hepatobiliary Disease, Zhongnan Hospital of Wuhan University, Wuhan 430071, Hubei Province, China xywjj08@163.com

PDF

530

被引次数

10

摘要：

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。

关键词: 脑死亡, 炎症因子, 凋亡, 蛋白激酶C, 肾脏移植

Abstract:

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 drill 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 gradually. 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 well 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.

中图分类号: