探讨家兔脑死亡后肝损伤机制。

健康雄性新西兰家兔60只，按随机数字表法随机分为脑死亡组和假手术组，每组30只。脑死亡组采用颅骨钻孔置管，缓慢间断颅内加压至脑死亡；假手术组颅骨钻孔置管，不加压。两组分别于术后2、6、8 h各处死10只，留取血标本及肝组织标本，采用比色法检测血清肝功能指标，苏木素-伊红（HE）染色观察肝脏的形态学改变，酶联免疫吸附试验（ELISA）检测血清中白介素（IL）-1β、肿瘤坏死因子（TNF）-α的水平。两组间数据比较采用t检验，组内各时间点比较采用方差分析及LSD-t检验。

脑死亡组家兔术后8 h的血清丙氨酸转氨酶（ALT）为（83±7）U/L，较术后6 h的（52±4）U/L明显升高（LSD-t=29.65，P<0.05）。随着时间延长，脑死亡组家兔肝脏水肿及汇管区炎症细胞浸润逐渐加重，术后8 h时出现中性粒细胞微脓肿，肝细胞受损不明显；而假手术组以中性粒细胞浸润为主。脑死亡组术后8 h血清IL-1β为（46±5）mg/L，较假手术组的（33±4）mg/L明显升高，差异有统计学意义（t=3.334，P<0.05）。脑死亡组术后2、6、8 h不同时间点血清TNF-α为（35.3±4.0）mg/L、（43.4±6.9）mg/L、（49.3±5.4）mg/L，均较对应假手术组的（25.4±3.1）mg/L、（24.2±7.1）mg/L、（25.4±2.0）mg/L明显升高，差异有统计学意义（t=3.409，3.369，7.224；P<0.05）。

脑死亡组家兔在术后8 h内肝功能及形态学无明显变化，术后8 h开始出现中性粒细胞微脓肿及汇管区淋巴细胞浸润，可能与免疫损伤有关。对于家兔脑死亡供体，宜8 h内行肝移植手术治疗。

To explore the mechanism of liver injury of rabbits after brain death.

Sixty healthy male New Zealand rabbits were randomly divided into brain death group (n=30) and sham group (n=30) according to the random number table. Rabbits in brain death group were put to brain death by cranial drilling, cathetering and increasing intracranial pressure in a slow, intermittent way. While rabbits in sham group underwent cranial drilling and cathetering without pressuring. Ten rabbits from each group were respectively put to death at the time points of 2, 6, 8 h after operation, and the samples of blood and liver tissues were collected. Serum indexes of liver function were detected by colorimetry. Morphology change of liver was observed by haematoxylin-eosin (HE) staining. The levels of interleukin (IL)-1β and tumor necrosis factor (TNF)-α were detected by enzyme linked immunosorbent assay (ELISA). The difference between two groups was compared using t test and the difference of each time points within the group was compared using variance analysis and LSD-t test.

The level of serum alanine aminotransferase (ALT) at 8 h after operation in brain death group was significant higher than that at 6 h after operation [(83±7)U/L vs. (52±4)U/L; LSD-t=29.65, P<0.05]. Liver edema and inflammatory cell infiltration in the portal area aggravated gradually in brain death group as time passed, neutrophil microabscess was observed at 8 h after operation and liver cell damage was found unobvious. While rabbits in sham group were found mainly with neutrophil infiltration. The level of serum IL-1β at 8 h after operation increased evidently in brain death group than that in sham group, and significant difference was observed [(46±5)mg/L vs. (33±4)mg/L; t=3.334, P<0.05]. The level of serum TNF-α at the time points of 2, 6, 8 h after operation increased evidently in brain death group than that in sham group, and significant difference was observed [(35.3±4.0)mg/L vs. (25.4±3.1)mg/L, (43.4±6.9) mg/L vs. (24.2±7.1)mg/L, (49.3±5.4)mg/L vs. (25.4±2.0)mg/L; t=3.409, 3.369, 7.224, P<0.05].

No obvious changes were observed in the liver function and morphology in brain death rabbits within 8 h after operation. Neutrophil microabscess and lymphocyte infiltration in the portal area were observed at 8 h after operation, which might be relevant with immunologic injury. It is ideal for donors of brain death rabbits to undergo liver transplantation within 8 h.