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目的 研究粘附分子在中性粒细胞介导的缺氧复氧大鼠心肌细胞损伤中的作用。方法 体外培养的大鼠心肌细胞缺氧６ 小时后复氧２ 小时。采用粘附试验和抗细胞间粘附分子－１（ｉｎｔｅｒｃｅｌｌｕｌａｒｃｅｌｌａｄｈｅｓｉｏｎ ｍ ｏｌｅｃｕｌｅ－１，ＩＣＡＭ－１）单克隆抗体阻断试验观察中性粒细胞与心肌细胞间的粘附作用和心肌细胞乳酸脱氢酶的释放。结果 缺氧６小时后复氧２小时可使心肌细胞与中性粒细胞粘附数显著增加（Ｐ＜ ０．０１），为正常培养组的１．７８ 倍；同时心肌细胞释放ＬＤＨ也明显增高（Ｐ＜ ０．０１）。５ μｇ／ｍ ｌ抗Ｉ－ＣＡＭ－１和抗淋巴细胞功能相关抗原－１（ＬＦＡ－１）单克隆抗体均可显著阻断中性粒细胞与心肌细胞间的粘附，阻断率为３６．７２％ 和３１．４１％ ，且心肌细胞释放ＬＤＨ明显下降（Ｐ＜ ０．０１）。结论 缺氧复氧后心肌细胞与中性粒细胞粘附增加，这种粘附作用伴随着中性粒细胞的激活和其细胞毒作用；抗ＩＣＡＭ－１ 和抗ＬＦＡ－１ 单抗能部分阻断这一粘附过程，提示粘附分子ＩＣＡＭ－１和ＬＦＡ－１ 参与介导中性粒细胞对缺氧复氧心肌细胞的损伤机制。抗ＩＣＡＭ－１ 和抗ＬＦＡ－１ 单抗可减轻中性粒细胞对缺氧复氧心肌细胞的损害
Objective To study the role of adhesion molecules in neutrophil-mediated hypoxia-reoxygenation cardiomyocyte injury in rats. Methods Rat cardiomyocytes cultured in vitro were reoxygenated for 6 hours after hypoxia for 6 hours. Adhesion test and intercellular adhesion molecule-1 (ICAM-1) monoclonal antibody blocking test was used to observe the adhesion between neutrophils and cardiomyocytes and myocardial cell lactate dehydrogenase Release. Results After 6 hours of hypoxia, reoxygenation for 2 hours could significantly increase the number of myocardial cells and neutrophils (P <0.01), which was 1.78 times higher than that in normal culture group. LDH release from myocardial cells was also significantly increased (P <0.01). 5 μg / ml anti-I-CAM-1 and anti-lymphocyte function associated antigen-1 (LFA-1) monoclonal antibody could significantly block the adhesion between neutrophils and cardiomyocytes with a blocking rate of 36 .72% and 31.41%, respectively, and the release of LDH from cardiomyocytes was significantly decreased (P <0.01). Conclusions After hypoxia-reoxygenation, the adhesion of myocardial cells to neutrophils increases. The adhesion is accompanied by the activation of neutrophils and its cytotoxicity. The anti-ICAM-1 and anti-LFA-1 monoclonal antibodies can partially block Discontinuation of this adhesion process suggests that the adhesion molecules ICAM-1 and LFA-1 are involved in mediating neutrophil injury in hypoxia-reoxygenation cardiomyocytes. Anti-ICAM-1 and anti-LFA-1 mAb reduce the damage of neutrophils to hypoxia-reoxygenation cardiomyocytes