抑肽酶对家兔全脑缺血-再灌注期白细胞介素-8基因的影响

目的 观察抑肽酶对家兔全脑缺血－再灌注期血清白细胞介素（IL）－8合成和释放的影响，并探讨其脑保护机制。方法 利用“六血管”阻断建立全脑缺血模型，24只家兔随机分为假手要组（A组），缺血－再灌注组（B组）和抑肽酶组（C组），每组8只兔。C组缺血30min再灌注4h,缺血前静注抑肽酶30000kIU/kg，随后每小时微量泵输注抑肽酶10000kIU/kg直至实验结束，B组为缺血－再灌注组，A组仅分离血管不阻断血流。分别在缺血前15min(10)及再灌注30min（R1）、2h（R2）和4h（R3）取颈内静脉血，测定血清IL－8浓度，实验结束取皮层苏木素－伊红染色，光镜观察白细胞浸润及神经元损伤程度。结果 C组IL－8随再灌注时间延长差异无显著性。B组由R1时的0.89ng/L迅速上升至R3时的1.46ng/L，分别增加2.28、2.97、3.74倍，同C组和A组相比差异有显著性；光镜下C组白细胞浸润及神经元损伤程度较B组明显减轻。结论 抑肽酶能有效抑制IL－8的合成和释放，这可能是抑肽酶减轻脑缺血－再 灌注损伤的重要机制。

Effect of aprotinin on interleukin-8 in rabbits following cerebr al ischemia-reperfusion injury

Objective　To observe the effects of apr otinin on the production and release of interleukin-8 (IL-8) following cerebra l ischemia-reperfusion and investigate its cerebral protective mechanism. Methods　Twenty-four rabbits were divided randomly into g roup A without occlusion of the vessels and aprotinin administration, group B wi th cerebral ischemia for 30 min and then with the reperfusion lasting 4 h, grou p C with aprotinin (30 000 kIU/kg) 10 min before occlusion and followed by 10 00 0 kIU*kg-1*h-1 intravenously till the end of procedure. A catheter was inserted into internal jugular bulb to obtain blood samples through the cat heter. The serum concentrations of IL-8 were measured 15 min (I0) befor e occlusi on, 30 min (R1), 2 h (R2) and 4 h (R3) after reperfusion. Hematorylin and eosin staining for cerebral tissue was processed to observe the leukocyte infilt ration and neuron damage. Results　The level of IL-8 was decreased in the group C as compared with that in the group B during reperfusio n (P＜0.05). IL-8 level in the group B was higher markedly during reperfusi on than that before ischemia and following reperfusion in the group A. Under lig ht microscopy, it was found that the leukocyte infiltration neuron damage were o bviously alleviated in the group C as compared with those in the group B. Conclusions　Aprotinin could effectively suppress the pro duction and release of IL-8, through which aprotinin could protect brain from i schemia and reperfusion injury.