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胸部撞击后肺组织细胞凋亡的变化及其意义 被引量:4

Changes and significance of lung cell apoptosis in rat after chest impact
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摘要 目的 探讨胸部撞击后肺损伤特点、肺组织细胞凋亡分布特征及其在肺损伤发生中的作用。方法 建立大鼠重度肺撞击伤模型,采用流式细胞术、免疫组化和形态学方法观察肺病理变化和细胞凋亡情况。结果 撞击侧肺(右肺)发生明显的出血、充血、水肿,光镜下可见肺组织较广泛的出血和结构破坏。对侧肺(左肺)伤情明显轻于右肺。伤后24 h双侧肺组织中细胞凋亡率均显著高于伤前水平(P<0.05)。右肺伤后48 h迅速升高,72 h达峰值,之后逐渐下降,伤后1周接近伤前水平。左肺组织细胞凋亡率显著低于右肺(P<0.05),在伤后48 h达高峰,72 h明显降低并接近伤前水平。右肺伤后24 h细胞凋亡以支气管、血管内皮和肺泡上皮为主,72 h以炎性细胞为主。结论 支气管、血管内皮和肺泡上皮是应力波作用的主要部位,该区域发生的细胞凋亡是肺水肿及继发性肺损伤的发生的重要原因之一。 Objective To explore the characteristics of lung injury, lung cell apoptosis and its significance in the injury. Methods An animal model of severe lung impact injury was established in Wistar rat by impacting the right chest. The pathological changes and cell apoptosis were observed with flow cytometry, immunochemical and other morphological methods. Results The right lung showed obvious hyperaemia, congestion and edema and with extensive blood extravasation and destruction of tissues, but only edema was seen in the left lung. The apoptotic rate in bilateral lung was significantly higher at 24th h post injury than that in pre injury ( P <0.01). The apoptotic rate in right lung rose rapidly at hour 48, reached a peak at hour 72 after the injury and then declined. It came to the normal level 1 week after injury. The rate of apoptosis in left lung reached a peak 48 h after injury and recovered obviously at 72 h, which was closed to pre injury level. Significant difference was found in the apoptosis between right lung and left lung ( P <0.05). The apoptotic cells in right lung were mainly bronchial, vascular endothelial and alveolar epithelial cells 24 h after the injury, and were inflammatory cells at the 72 nd h. Conclusion The stress wave mainly affects bronchial, vascular endothelia and alveolar epithelia, so the apoptosis in these regions is one of major causes of lung edema and secondary injury after impact.
出处 《第三军医大学学报》 CAS CSCD 北大核心 2001年第2期193-195,共3页 Journal of Third Military Medical University
基金 国家自然科学基金
关键词 细胞凋亡 胸部撞击伤 肺组织 lung impact injury apoptosis
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