Characteristics of neutrophils infiltration in ventilation-induced lung injury
Characteristics of neutrophils infiltration in ventilation-induced lung injury
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DOI：
10.1007/s11596-012-1044-0
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发表时间：
2012-12-01
影响因子：
--
通讯作者：
Liu, Yang
中科院分区：
文献类型：
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作者：
Wang, Yuelan;Dai, Guofeng;Liu, Yang
中性粒细胞在通气诱导的肺损伤中起关键作用。探讨大潮气量通气时中性粒细胞内流的特点。麻醉大鼠随机分为低潮气量通气组（Vt：7 mL/kg，LV组）和大潮气量通气组（Vt：42 mL/kg，HV组），每组40只。各组大鼠分别通气0、60、90、120和240 min，测定肺湿/干重比（W/D）。采用酶联免疫吸附法（ELISA）检测巨噬细胞炎性蛋白-2（MIP-2）、肿瘤坏死因子-α（TNF-α）水平及髓过氧化物酶（MPO）活性。经瑞氏染色后计数支气管肺泡灌洗液（BALF）中性粒细胞数，计算肺组织中性粒细胞百分比。组织学检查观察不同通气方式后肺组织的变化。结果表明，HV组肺湿重比（W/D）在90、120和240 min时均明显增加，MIP-2和TNF-α水平在120和240 min时均明显升高，BALF中性粒细胞和肺组织中性粒细胞百分比在120和240 min时也明显升高，与肺组织MPO活性的增强相一致。HV组肺损伤与通气时间及肺内中性粒细胞浸润密切相关。总之，在通气诱导的肺损伤中，中性粒细胞浸润以时间依赖性的方式存在，并且与肺损伤的加重相关。肺结构损伤可能是机械通气所致肺损伤的主要原因。
Neutrophils play a critical role in ventilation-induced lung injury. This study was aimed to investigate the characteristics of neutrophils influx in lungs induced by high tidal volume ventilation. Anaesthetized rats were randomly divided into low tidal volume ventilation group (Vt: 7 mL/kg, LV group) or high tidal volume ventilation group (Vt: 42 mL/kg, HV group) (n=40 in each). Rats in each group were ventilated for 0, 60, 90, 120 and 240 min. The wet/dry lung weight ratio (W/D) was measured. The levels of macrophage inflammatory protein-2 (MIP-2) and tumor necrosis factor-alpha (TNF-alpha), and the activity of myeloperoxidase (MPO) were detected by enzyme-linked immunosorbent assay (ELISA). The number of neutrophils in bronchoalveolar lavage fluid (BALF) was counted after Wright's staining, and the percentage of netrophils in lung tissues calculated. Histopatholgical examination was used to observe the changes of lung tissues after different ventilations. The results showed that the W/D weight ratio was increased, and the levels of MIP-2 and TNF-alpha significantly enhanced in HV group at 90, 120 and 240 min. Neutrophils in BALF and the neutrophil percentage in lung tissues were also elevated at 120 and 240 min, which coincided with the enhanced activity of MPO in HV group. The lung injury was significantly related with the ventilation time and the infiltration of neutrophils in lungs in HV group. In conclusion, in ventilation-induced lung injury, neutrophil infiltration is present in a time-dependent manner and associated with the aggravated lung injury. Pulmonary structural damage may be the main reason for ventilation-induced lung injury.