摘要
目的 :动态观察兔胸部撞击伤时中性粒细胞 (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 ,分离纯化肺灌洗液中的 PMN,应用流式细胞术测定 PMN凋亡、坏死、存活细胞比例及呼吸爆发功能的变化 ,并且观察与乳酸脱氢酶 (L DH)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 12小时 ,在伤后各时间点活细胞增多 ;而肺灌洗液 PMN呼吸爆发从伤后 2小时即显著增强 ,8小时达到峰值 ;同时肺灌洗液 L DH的升高在伤后 4～ 2 4小时显著高于正常对照组 ;伤后 PMN胞浆游离 Ca2 +有短暂升高。结论 :胸部撞击伤时 ,PMN在肺组织中大量扣押 ,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凋亡延迟可能与胞浆游离 Ca2
Objective:To investigate the relationship between the regulation of polymorphonuclear neutrophil (PMN) apoptosis and the lung injury after chest impact trauma.Methods:The rabbits were subjected to chest impact trauma.PMNs were purified from bronchoalveolar lavage fluid and their apoptosis,necrosis,survival and respiratory burst were detected by flow cytometry.Meanwhile,lactate dehydrogenase(LDH) and intracellula free Ca 2+ levels in PMN were also measured.Results:The delayed apoptosis of PMNs in bronchoalveolar lavage fluid was observed from 2 hours to 12 hours after trauma,and the number of viable cells increased.Respiratory burst of PMNs in bronchoalveolar lavage fluid was significantly increased at 2 hours and peaked at 8 hours after trauma.Meanwhile,LDH levels in bronchoalveolar lavage fluid were higher compared with controls from 4 hours to 24 hours ( P <0 05 or P <0 01),while intracellular free Ca 2+ in PMN was increased temporally.Conclusions:Retention of PMN in tissues and the abnormality in apoptotic pathway might result in persistent activation of PMN and excessive release of toxic substances,thereby contributing to tissue injury.The temporal elevation of intracellular free Ca 2+ could be responsible for the delayed apoptosis of PMN.
出处
《中国危重病急救医学》
CAS
CSCD
2002年第2期83-86,共4页
Chinese Critical Care Medicine
关键词
胸部撞击伤
中性粒细胞
凋亡
呼吸爆发
继发性肺损伤
chest impact trauma
polymorphonuclear neutrophil
apoptosis
respiratory burst
secondary lung injury
