Chinese Journal of Tissue Engineering Research ›› 2012, Vol. 16 ›› Issue (53): 10021-10026.doi: 10.3969/j.issn.2095-4344.2012.53.027

Previous Articles     Next Articles

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

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.

CLC Number: