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为进一步探讨脑缺血再灌注时的神经免疫变化，采用动物实验方法对肿瘤坏死因子（TNF）和可溶性白细胞介素-2受体（sIL-2R）进行了动态观察。选用新西兰白兔建成Pulsinelli四血管缺血模型，以放免法分别测定了缺血再灌注后1、4、10、24h血浆血栓素B2（TXB2）、TNF、sIL－2R的水平。结果显示：缺血再灌后TXB2、TNF、SIL－2R均显著升高。缺血1h后TNF即升高至185fmol／L（实验前为120fmol／L），增高呈持续性，以10h为最高（247fmol／L）。sIL－2R的增高以缺血再灌注后1、4、24h为著。TNF的增高与TXB2呈正相关（r=0．9317，P＜0．05）。以上结果提示急性脑缺血再灌注后的TNF表达增高，这可能是由于血管内皮损伤和神经组织缺血后合成增加所致，其作用可能与诱导免疫过程中SIL－2R的产生有关。TNF与TXB2相关性改变表明，缺血再灌注后的神经免疫的变化可能与白细胞—血管内皮细胞—血小板环路的激活有关。
In order to further explore the neuroimmunological changes during cerebral ischemia-reperfusion, the dynamic changes of tumor necrosis factor (TNF) and soluble interleukin-2 receptor (sIL-2R) were observed by animal experiments. Pulsinelli four-vessel ischemia models were established in New Zealand white rabbits. The levels of TXB2, TNF and sIL-2R were determined by radioimmunoassay at 1, 4, 10 and 24 hours after ischemia-reperfusion. The results showed that: TXB2, TNF, SIL-2R were significantly increased after ischemia-reperfusion. After 1h of ischemia, TNF increased to 185fmol / L (120fmol / L before the experiment), increased continuously, and reached the peak at 10h (247fmol / L). The increase of sIL-2R is related to 1,4,24 h after ischemia-reperfusion. The increase of TNF was positively correlated with TXB2 (r = 0.9317, P <0.05). The above results suggest that the TNF expression increased after acute cerebral ischemia-reperfusion, which may be due to vascular endothelial injury and increased synthesis of nerve tissue after ischemia, its role may be related to the induction of immune process SIL-2R production. The correlation between TNF and TXB2 indicates that the change of neuroimmunity after ischemia-reperfusion may be related to the activation of leukocyte-vascular endothelial cell-platelet loop.