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目的：通过大鼠烟雾吸入伤血清体外刺激培养的内皮细胞和中性粒细胞（ＰＭＮ），了解ＰＭＮ粘着的变化，以及抗ＣＤ１１ａ、抗ＣＤ１１ｂ和抗ＩＣＡＭ－１对ＰＭＮ粘着的影响，探讨粘附因子在烟雾吸入性损伤中的作用。方法：在体外实验中用荧光标记ＰＭＮ，测定ＰＭＮ与烟雾吸入性损伤血清刺激的内皮细胞的粘着率，并采用抗体阻断技术，测定了粘附因子ＣＤ１１ａ、ＣＤ１１ｂ和ＩＣＡＭ－１在ＰＭＮ粘着的作用。结果：吸入伤血清能使粘着率增高，１２～２４ｈ是正常时的３倍多，ＰＭＮ的内皮细胞粘附因子抗体（抗ＣＤ１１ａ、抗ＣＤ１１ｂ和抗ＩＣＡＭ－１）减少ＰＭＮ与内皮细胞粘着率（４４％、５５％和５１％）。结论：烟雾吸入伤血清能增加ＰＭＮ的粘着，其可能是ＰＭＮ浸润的病理基础，进一步研究证明，粘附因子ＣＤ１１ａ、ＣＤ１１ｂ和ＩＣＡＭ－１在ＰＭＮ浸润过程中起重要作用，而且浸润的中性粒细胞释放氧自由基和蛋白酶能导致进一步的肺组织损害。
OBJECTIVE: To investigate the changes of PMN adhesion and the effects of anti-CD11a, anti-CD11b and anti-ICAM-1 on the adhesion of PMN by stimulating the cultured endothelial cells and neutrophils (PMN) The role of factors in smoke inhalation injury. Methods: PMN was detected by fluorescence in vitro and the adhesion rate of endothelial cells stimulated by PMN and smoke inhalation injury was measured. Antibody blocking technique was used to determine the adhesion of CD11a, CD11b and ICAM-1 to PMN effect. Results: Inhalation of wound serum increased the adhesion rate, which was more than 3 times of the normal value at 12 to 24 hours. The adhesion of PMN to anti-CD11a, anti-CD11b and anti-ICAM-1 decreased the adhesion of PMN to endothelial cells 44%, 55% and 51%). Conclusion: Inhalation of smoke can increase the adhesion of PMN, which may be the pathological basis of PMN infiltration. Further studies have shown that the adhesion molecules CD11a, CD11b and ICAM-1 play an important role in PMN infiltration, and infiltrating neutrophils Cells release oxygen free radicals and proteases can lead to further lung tissue damage.