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通过将兔肺挫伤后胸壁“开窗”方法，直接在显微镜下观察肺挫伤后肺微循环障碍和肺水肿的发生、发展过程，以及血清、肺组织和支气管肺泡灌洗液（ＢＡＬ）中磷脂酶Ａ２（ＰＬＡ２）变化，探讨肺挫伤后ＰＬＡ２在肺微循环障碍和肺水肿中的作用机制。实验发现：肺挫伤后１～２小时肺表面小动脉收缩，继之扩张、充血，个别肺小动脉栓塞。肺水肿可在肺挫伤后１～２小时出现，其发展形式有两种：一种是以肺泡水肿为主，另一种是以间质水肿为主。ＰＬＡ２在肺挫伤后２小时开始升高，４～５小时达到高峰，肺组织和ＢＡＬ中ＰＬＡ２活性亦升高。肺内的细胞浸润、聚集。应用ＰＬＡ２抑制剂氯喹后，ＰＬＡ２活性降低，肺微循环改善，肺水肿减轻。提示：ＰＬＡ２在肺挫伤后肺微循环障碍和肺水肿的形成、发展中起重要作用
The pulmonary microcirculation and pulmonary edema after pulmonary contusion were observed under a microscope directly through the method of “fenestration” of the chest wall after contusion of rabbits. The development of phospholipid in serum, lung tissue and bronchoalveolar lavage fluid (BAL) Enzyme A2 (PLA2) changes in lung PLA2 after pulmonary contusion and pulmonary edema in the mechanism of action. The experiment found: 1 ~ 2 hours after pulmonary contusion pulmonary artery surface contraction, followed by expansion, congestion, and individual pulmonary arterial embolization. Pulmonary edema in the pulmonary contusion 1 to 2 hours after the emergence of its development in two forms: one is the main alveolar edema, and the other is mainly based on interstitial edema. PLA2 began to rise 2 hours after pulmonary contusion, peaked at 4 to 5 hours, and PLA2 activity also increased in lung tissue and BAL. Infiltration of the lung cells, aggregation. After application of chloroquine, a PLA2 inhibitor, PLA2 activity was reduced, pulmonary microcirculation was improved, and pulmonary edema was relieved. Tip: PLA2 plays an important role in the formation and development of pulmonary microcirculation and pulmonary edema after pulmonary contusion