[1]肖桃元,王久惠,陶忠芬,等.大鼠肺放射性损伤的超微结构观察[J].第三军医大学学报,2007,29(21):2034-2037.
 XIAO Tao-yuan,WANG Jiu-hui,TAO Zhong-fen,et al.Ultrastructure of radiation-induced pulmonary injury in rats[J].J Third Mil Med Univ,2007,29(21):2034-2037.
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《第三军医大学学报》[ISSN:1000-5404/CN:51-1095/R]

卷:
29卷
期数:
2007年第21期
页码:
2034-2037
栏目:
论著
出版日期:
2007-11-15

文章信息/Info

Title:
Ultrastructure of radiation-induced pulmonary injury in rats
作者:
肖桃元王久惠陶忠芬韦建可金星李涛路菊田路谭永红
第三军医大学:高原军事医学系中心实验室,大坪医院野战外科研究所肿瘤中心; 四川省肿瘤医院内科
Author(s):
XIAO Tao-yuan WANG Jiu-hui TAO Zhong-fen WEI Jian  KE Jin-xing LI Tao LU Ju TIAN Lu TAN Yong-hong
Laboratory Center, College of High Altitude Military Medicine, Chongqing 400038, Oncology Center, Institute of Surgery Research, Daping Hospital, Third Military Medical University,  Chongqing 400042; Medical Department, Oncology Hospital of Sichuan Province, Chengdu 610041, China
关键词:
放射损伤超微病理大鼠
Keywords:
radiation injury ultrapathology lung rat
分类号:
R322.35; R818.021
文献标志码:
A
摘要:
目的  观察放射性肺损伤的超微病理变化,并探讨放射性肺炎和肺纤维化的发生机制。 方法  SD雄性大鼠77只,分实验组63只和正常对照组14只,实验组用8 MV直线加速器30、20、10 Gy 3个剂量一次性照射右半胸,左半胸作为实验对照,分7个时相点(1、3、7、14、28、90、180 d)活杀动物,取右肺中叶组织作光、电镜观察。  结果  各实验组放射损伤早期(1~30 d)Ⅰ型上皮损伤,吞噬细胞增多、活跃;Ⅱ型上皮激活;肺泡隔毛细血管内皮损伤、增生,血小板、红细胞聚集,微血栓形成;间质水肿。后期(60~180 d)Ⅱ型上皮异常增殖,成纤维细胞/胶原增生,血管萎缩减少,肺泡纤维化。各实验组损伤病变程度与照射剂量相关。  结论  肺泡隔血管内皮病变、血液循环障碍和间质水肿是放射性肺损伤早期的主要病理变化,是肺纤维化的始动因素;成纤维细胞激活、Ⅱ型上皮细胞异常增殖、吞噬细胞等分别参与肺纤维化进程, 是多种因素综合作用的结果。
Abstract:
Objective    To investigate ultrastructural pathology and pathogenesis of radiation-induced pulmonary injury.    Methods    Sixty-three adult male SD rats were divided in three groups randomly, receiving irradiation at dose of 10, 20, and 30 Gray at their right hemithorax. The irradiated rats of each group were killed at 1, 3, 7, 14, 28, 90, 180 d, and their lungs were observed by light and electron microscope. Another 14 rats served as normal control.     Results    In early phase of irradiation-induced injury (1-30 d), we observed type Ⅰ pneumocytes injury, increased and activated macrophages, the activation of type Ⅱ pneumocytes, the damage and proliferation of endothelial cells, the congregation of platelet and RBC, thrombosis, and interstitial edema. In the fibrotic phase (60-180 d), there were the abnormal proliferation of type Ⅱ pneumocytes, the proliferation of fibroblasts and collagens, the atrophy and depletion of capillary vessels, and finally lung fibrosis.    Conclusion    The pathological changes in endothelial cells of capillary vessels, the disturbance of blood circulation and interstitial edema are the early major pathological changes of irradiation-induced pulmonary injury, which may be the primal factors responsible for the development of irradiation-induced lung fibrosis. The process of lung fibrosis involves  fibroblast activation, abnormal proliferation of type Ⅱ pneumocytes and increased macrophages, resulting from the combined effects of complex factors.

参考文献/References:

肖桃元,王久惠,陶忠芬,等.  大鼠肺放射性损伤的超微结构观察[J]. 第三军医大学学报, 2007, 29(21):2034-2037.

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更新日期/Last Update: 2008-07-02