摘要
目的 探讨内皮素 (Endothelin ,ET)和一氧化氮 (NO)在烧冲复合伤肺损伤中的作用及可能机制。方法 制作大鼠烧冲复合伤模型 ,用 99Tcm 人聚巨蛋白 ( 99Tcm macro aggregatedalbumin ,99Tcm MAA)标记方法观察肺部血液循环状况和肺血管通透性 ,并检测血液流变学和动脉血气变化 ;分别用ET受体 (ETR)拮抗剂PD 14 2 893和NO合酶 (NOS)抑制剂硝基左旋精氨甲酯 (Nitro L argininemethylester ,L NAME)干预 ,观察其对上述与肺损伤密切相关的指标变化。结果 烧冲复合伤大鼠全血粘度、动脉血气分析、支气管肺泡灌洗液 (Bronchoalveolarlavagefluid ,BALF)放射性活性和肺部血液循环状况均出现了显著变化 (P <0 .0 5 ) ,给予PD 14 2 893和L NAME分别可减轻和加重这些指标的变化 (P <0 .0 5 )。结论 烧冲复合伤大鼠可出现明显肺损伤 ,ET和NO通过多种途径影响烧冲复合伤肺损伤的发生和发展。
Objective To study the roles of endothelin (ET) and nitric oxide (NO) in pulmonary tissue damage after combined burn blast injury and the mechanisms. Methods After establishment of animal model of combined burn blast injury in rats, blood circulation in pulmonary tissues and the permeability of pulmonary vessels were observed by 99 Tc m macro aggregated albumin labeling assay. Hemorheological changes were determined and arterial blood gas analysis was performed. After administration of ET receptor (ETR) antagonist PD 142893 and NO synthase (NOS) inhibitor (nitro L arginine methyl ester, L NAME), the above parameters were also detected. Results There were significant changes in blood viscosity, blood gas analysis, radioactivity in bronchoalveolar lavage fluid and blood circulation in pulmonary tissues in rats with combined burn blast injury( P <0.05). PD 142893 ameliorated the pulmonary injury but L NAME deteriorated the changes( P <0.05). Conclusion Combined burn blast injury can lead to pulmonary tissue damage. ET and NO participate in the damages via different pathways.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2003年第15期1361-1364,共4页
Journal of Third Military Medical University
关键词
内皮素
一氧化氮
烧冲复合伤
肺脏
endothelin
nitric oxide
combined burn blast injury
pulmonary