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为探讨高渗氯化钠羟乙基淀粉 4 0溶液 (HSH)复苏失血性休克时对肺部炎症免疫调节作用的分子机制 ,采用SD大鼠失血性休克 +气管内滴入内毒素 (LPS)的二次打击模型。分别用HSH和乳酸林格液 (RL)复苏大鼠 ,复苏后 1、2、4h处死动物 ,流式细胞仪检测中性粒细胞 (PMN)上CD11b的表达 ;支气管肺泡灌洗液计数PMN ;Bradly改良法测定肺组织髓过氧化物酶 (MPO)活性以反映肺总的PMN浸润。结果显示 ,HSH组同RL组比较 ,各时间点PMN表达的CD11b显著下降 (P <0 0 1) ,BALF中PMN减少 ,肺水肿程度减轻 ,肺MPO活性水平降低(P <0 0 5 )。提示HSH可抑制LPS诱导的PMN粘附分子CD11b上调表达 ,减少肺内PMN的浸润数 ,减轻过度炎症反应 ,对肺组织具有保护性的抗炎效果。
To investigate the molecular mechanism of hypersensitive sodium chloride hydroxyethyl starch 40 solution (HSH) in the immune regulation of lung inflammation in hemorrhagic shock, the effects of hemorrhagic shock + intratracheal instillation of endotoxin (LPS) The second strike model. Rats were resuscitated with HSH and lactated Ringer ’s solution (RL) respectively. Animals were sacrificed at 1, 2 and 4 hours after resuscitation. The expression of CD11b on neutrophils (PMN) was detected by flow cytometry. The bronchoalveolar lavage fluid was counted for PMN. Bradly’s modified method was used to determine myeloperoxidase (MPO) activity in the lung to reflect the total lung PMN infiltration. The results showed that CD11b expression in PMN was significantly decreased in HSH group compared with RL group (P <0.01), PMN decreased in BALF, pulmonary edema lessened and lung MPO activity decreased (P <0.05). These results suggest that HSH can inhibit LPS-induced PMN adhesion molecule CD11b upregulation, reduce the number of PMN infiltration in the lung, relieve excessive inflammatory reaction and have protective anti-inflammatory effect on lung tissue.