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目的：中性粒细胞粘附在缺血再灌注损伤中有非常重要的作用。本文用ＳＤ大鼠趾长屈肌缺血再灌注损伤模型，观察Ｌ一粘附素单抗ＬＡＭ１—１１６在缺血再灌注损伤中的作用。方法：３０只ＳＤ大鼠被均分为２组：ＬＡＭ１—１１６组和生理盐水对照组。每只大鼠的一侧趾长屈肌作为正常对照，另外一侧进行 ３ ｈ缺血 ４ ｈ再灌注。结果：ＬＡＭ１— １１６组实验侧的髓过氧化物酶为正常的２倍（２．３±２．２），生理盐水对照组则为正常的２８倍（２７．５±１１．７）（Ｐ＜０．００１）；ＬＡＭ１—１１６组的湿重比（１．１０± ０．１０）、疲劳肌力（７７． １％±１２．１％）与对照组相比（分别为 １． ２３± ０． １０和 ４９． ７％± ９ ．３％）明显改善（Ｐ＜ ０．０５）；组织学上，ＬＡＭ１—１１６组的中性粒细胞局部浸润显著减少，水肿减轻。结论：通过 Ｌ－粘附素单克隆抗体 ＬＡＭ１— １１６阻断 Ｌ－粘附素的功能，可以有效地降低中性粒细胞在再灌注肌肉中的浸润，防止组织水肿，从而改善肌肉的功能。
OBJECTIVE: Neutrophil adhesion plays a very important role in ischemia-reperfusion injury. In this paper, SD rats with long flexor myoelectric injury model was used to observe the role of L-adriamycin LAM1-116 in ischemia-reperfusion injury. Methods: Thirty SD rats were divided into two groups: LAM1-116 group and saline control group. The long flexor flexor of each rat was used as a normal control, and the other side was reperfused for 4 h at 4 h after ischemia. RESULTS: Myeloperoxidase was twice as normal (2.3 ± 2.2) in the LAM1-116 group and 28 times (27.5 ± 11.7) in the saline control group (P <0.001). The wet weight ratio (1.10 ± 0.10) and fatigue muscle strength (77.1% ± 12.1%) in LAM1-116 group were significantly lower than those in control group (1.23 ± 0. 10 and 49. 7% ± 9. 3%) was significantly improved (P <0.05). Histologically, the local infiltration of neutrophils in LAM1-116 group was significantly reduced and edema was relieved. CONCLUSION: The blocking of the function of L-adhesin by L-1 -16 monoclonal antibody can effectively reduce the infiltration of neutrophils in reperfused muscle and prevent the edema of tissues, thus improving muscle function.