缺血-再灌注过程中白细胞与内皮细胞粘附机制探讨  

Study on the mechanism of leukocytes adherence to endothelial cells during ischemia-reperfusion

作　　者：康舟军[1] 梅冰[1] 杨瑞和[1] 

机构地区：[1]第二军医大学长海医院急诊科,上海200433

出　　处：《上海医学》2002年第12期770-772,共3页Shanghai Medical Journal

摘　　要：目的　研究缺血 -再灌注过程中白细胞与内皮细胞粘附增强的分子机制。方法　采用Lamson’s法造成兔失血性休克 (血压为 6kPa ,1kPa =7.5mmHg) ,1.5h后再经颈静脉回输所失血液 ,分别于失血前 (对照组 )、失血 1.5h(休克组 )、再灌注 3h后 (再灌注组 )抽血分离中性粒细胞 (PMN) ,并测定其粘附分子CD18。结果　对照组PMNCD18的表达为 ( 1.62± 0 .2 6)× 10 -3A·min-1·μg蛋白 -1,休克组的表达为 ( 1.76± 0 .3 4)×10 -3A·min-1·μg蛋白 -1,再灌注组的表达为 ( 3 .2 4± 0 .2 8)× 10 -3A·min-1·μg蛋白 -1。再灌注组PMNCD18的表达与休克组及对照组比较 ,差异有显著性 (P <0 .0 1)。结论　缺血 -再灌注过程中 。Objective To study the molecular mechanism of increasing leukocytes adherence to the endothelial cells during ischemia-reperfusion. Methods Hemorrhagic shock(BP 6kPa) was induced by Lamson's method, and the blood was reinfused through jugular vein after 1.5 h. The polymorphonuclear leukocytes(PMN) were separated and the adhension molecule CD18 was detected before the blood loss ( control group), 1.5 hours after hemorrhagic shock(shock group) and 3 hours after reperfusion(reperfusion group). Results The expression of PMN CD18 was (1.62 ±0.26)×10 -3 A·min -1·μg -1protein in the control group,(1.76±0.34)×10 -3 A·min -1·μg -1protein in shock group, and (3.24±0.28)×10 -3 A·min -1·μg -1protein in reperfusion group.The variance between reperfusion group and the shock group with the control group was remarkable(P<0.01). Conclusion The increase of the leukocytes adherence to endothelial cells during ischemia-reperfusion is due to increase of the expression of PMN CD18.

关 键 词：中性粒细胞粘附分子 缺血-再灌注过程 白细胞 内皮细胞粘附 机制 

分 类 号：R363[医药卫生—病理学]