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作 者:夏瑞[1] 杨光[2] 卢娟[1] 夏中元[2] 侯望平[2] 夏正远[2]
机构地区:[1]湖北省荆州市第一人民医院麻醉科,434000 [2]武汉大学人民医院麻醉科
出 处:《中华实验外科杂志》2001年第2期167-168,T003,共3页Chinese Journal of Experimental Surgery
摘 要: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 ,2 4只家兔随机分为假手术组 (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 3 0min再灌注 4h ,缺血前静注抑肽酶 3 0 0 0 0kIU/kg ,随后每小时微量泵输注抑肽酶 10 0 0 0kIU/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(I0 )及再灌注 3 0min(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 .2 8、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Objective To observe the effects of aprotinin on the production and release of interleukin 8 (IL 8) following cerebral ischemia reperfusion and investigate its cerebral protective mechanism. Methods Twenty four rabbits were divided randomly into group A without occlusion of the vessels and aprotinin administration, group B with cerebral ischemia for 30 min and then with the reperfusion lasting 4 h, group C with aprotinin (30 000 kIU/kg) 10 min before occlusion and followed by 10 000 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 catheter. The serum concentrations of IL 8 were measured 15 min (I 0) before occlusion, 30 min (R 1), 2 h (R 2) and 4 h (R 3) after reperfusion. Hematorylin and eosin staining for cerebral tissue was processed to observe the leukocyte infiltration and neuron damage. Results The level of IL 8 was decreased in the group C as compared with that in the group B during reperfusion ( P <0.05). IL 8 level in the group B was higher markedly during reperfusion than that before ischemia and following reperfusion in the group A. Under light microscopy, it was found that the leukocyte infiltration neuron damage were obviously alleviated in the group C as compared with those in the group B. Conclusions Aprotinin could effectively suppress the production and release of IL 8, through which aprotinin could protect brain from ischemia and reperfusion injury.
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