中性粒细胞凋亡与体外循环全身炎性反应相关性研究

目的探讨中性粒细胞（polymorphonuclear neutrophil,PMN）凋亡与体外循环（extracorporeal circulation,ECC）全身炎性反应的相关性及意义。方法50例ECC心脏直视手术病人,于ECC前、ECC结束时、ECC结束后4h、术后第1d晨四个时点采取静脉血,以全血细胞计数仪测定PMN数量,流式细胞仪测定PMN凋亡率和PMN表面粘附分子CD11b表达变化,ELISA法测定血浆弹性蛋白酶浓度,透射电镜观察PMN凋亡细胞形态学变化。结果PMN凋亡率在ECC期间明显降低,与ECC时间呈负相关。PMN数量、CD11b表达、血浆弹性蛋白酶浓度在ECC期间明显升高,与其凋亡率呈负相关,且血浆弹性蛋白酶浓度与ECC时间呈正相关。透射电镜下可见典型的PMN凋亡细胞。结论ECC导致PMN的凋亡受抑数量增加、生存周期延长、CD11b表达上调、脱颗粒释放弹性蛋白酶增加,加剧炎性反应扩散和组织损伤,炎性反应进一步迁延。

Correlation between Polymorphonuclear Neutrophil Apoptosis and Systemic Inflammatory Response to Extracorporeal Circulation

OBJECTIVE To investigate the correlation and significance between polymorphonuclear neutrophil （PMN） apoptosis and systemic inflammatory response to extracorporeal circulation （ECC）. METHODS Fifty patients undergoing open heart surgery with ECC were studied. Blood samples were drawn from the central venous line before starting ECC, at the end of the ECC, 4 hours after ECC and on the frist postoperative morning. The PMN counts were performed by blood cell counter. PMN were isolated, and its apoptosis and the expression of CD1 1b were evaluated by flow cytometry. The plasma concentration of elastase was determined by enzyme - linked immunosorbentassays. The morphological change of PMN apoptosis was detected by transmission electron microscope. RESULTS The rates of PMN apoptosis were significantly reduced during ECC until the frist postoperative morning, and the rate at 4 hours after ECC negatively correlated with the duration of ECC. The PMN counts,the expression of PMN CDllb and the levels of plasma elastase were markly increased during ECC, and at 4 hours after ECC inversely correlated with PMN apoptosis rate. Peak elastase levels correlated positively with the duration of ECC. PMN apoptosis was showed under electron microscope. CONCLUSION ECC suppress PMN apoptosis,increase PMN count, and prolong the functional lifespan of PMN. The inhibition of PMN apoptosis cause upregulation of PMN CD11 b expression and elevation of plasma PMN elastase level, potentiate and prolong the systemic inflammation response induced by ECC.