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目的 :PMN在炎症的发生、发展和转归中起着至关重要的作用 ,本实验动态地观察兔胸部撞击伤时PMN凋亡的发生以及与肺损伤之间的关系.方法 :制备兔胸部撞击伤模型 ,分离纯化灌洗液中的PMN ,应用流式细胞术测定凋亡、坏死、存活细胞比例及呼吸爆发功能的变化 ,并且观察与LDH和胞浆游离Ca2 +变化之间的关系.结果 :肺灌洗液中PMN的凋亡延迟持续至 1 2h ,在伤后各时相点活细胞增多.而灌洗液PMN呼吸爆发从 2h即显著增强 ,8h达到峰值.同时 ,灌洗液LDH的升高从 4h~2 4h显著高于对照.伤后PMN胞浆游离Ca2 +有短暂升高.结论 :PMN在肺组织中大量扣押并且正常的凋亡途径发生障碍 ,造成PMN持续处于激活状态及毒性内容物的持续释放 ,与肺组织损伤有密切关系 ,并且PMN凋亡延迟可能与Ca2 +的短暂升高有关.“,”Objective:PMN, one of the most important inflammatory cells, functions throughout the initiation, progression and resolution of inflammation. This study was designed to examine the relationship between the regulation of PMN apoptosis and the lung injury after chest impact trauma. Methods:PMNs were purified after the chest impact trauma model in rabbits was reproduced, and their apoptosis, necrosis, survival and respiratory burst were detected by flow cytometry. Meanwhile, LDH and [Ca 2+ ]i were measured. Results:The delayed apoptosis of PMNs in bronchoalveolar lavage fluid was observed from 2h to 12h after trauma, and viable cells increased. Respirtory burst of PMNs in bronchoalveolar lavage fluid was increased significantly from 2h, approached peak value at 8h. Meanwhile, LDH in bronchoalveolar lavage fluid were higher than control (P<0.05) from 4h to 24h, and intracellular free Ca 2+ in PMN was increased temporally. Conclusions:Retention of PMN in tissues and the abnormality in apoptotic pathway inevitably generate persistent activation of PMN and excessive release of toxic substances, resulting in tissue injury. The temporal increasing of intracellular free Ca 2+ may be responsible for the delayed apoptosis of PMN. [