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乌司他丁对肝缺血-再灌注后急性肺损伤的保护作用
引用本文:王晓琳,张宏,刘荣,王和玫. 乌司他丁对肝缺血-再灌注后急性肺损伤的保护作用[J]. 中国危重病急救医学, 2003, 15(7): 432-434
作者姓名:王晓琳  张宏  刘荣  王和玫
作者单位:1. 解放军总医院,北京,100853
2. 军事医学科学院六所二室,北京,100850
基金项目:全军医药卫生科研基金资助项目 ( 0 1MB0 76)
摘    要:
目的 :观察肝缺血再灌注后急性肺损伤的发病机制及乌司他丁的干预作用。方法 :建立大鼠部分肝缺血再灌注模型 ,随机分为手术对照组 (对照组 ) ,肝缺血 90 min组 (缺血组 ) ,肝缺血 90 m in、再灌注 12 0 m in组 (再灌注组 ) ,缺血前 30 m in静脉注射乌司他丁 +肝缺血 90 min、再灌注 12 0 min组 (乌司他丁组 )。检测支气管肺泡灌洗液 (BAL F)中总蛋白含量、肺组织干 /湿质量比 (D/ W)、肺组织髓过氧化物酶 (MPO)含量及血浆中丙二醛 (MDA)含量。结果 :1与对照组比较 ,肝缺血再灌注损伤后各组大鼠 BAL F中总蛋白含量均明显升高(P<0 .0 5或 P<0 .0 1) ,再灌注组总蛋白升高更为明显 ,乌司他丁能干预其升高 ;肺 D/ W则均明显降低(P均 <0 .0 1) ,乌司他丁能干预其降低程度。 2随着肝缺血再灌注的发生 ,肺组织 MPO与血浆 MDA含量均逐渐升高 ,以再灌注组升高更明显 (P均 <0 .0 1) ,乌司他丁能干预 MDA和 MPO的升高。结论 :肝缺血再灌注后急性肺损伤的主要病理生理过程是氧化抗氧化系统的失衡 ,中性粒细胞是肺组织急性损伤的主要炎性细胞 ;乌司他丁通过抑制中性粒细胞在肺组织中的渗出及其抗氧化作用显著减轻急性肺损伤的程度。

关 键 词:肺损伤,急性 多器官衰竭 缺血-再灌注损伤,肝 蛋白酶抑制剂
文章编号:1003-0603(2003)07-0432-03
修稿时间:2003-02-21

Protective effect of a protease inhibitor on acute lung injury after hepatic ischemia/reperfusion in the rat
WANG Xiaolin ,ZHANG Hong ,LIU Rong ,WANG Hemei .. Protective effect of a protease inhibitor on acute lung injury after hepatic ischemia/reperfusion in the rat[J]. Chinese critical care medicine, 2003, 15(7): 432-434
Authors:WANG Xiaolin   ZHANG Hong   LIU Rong   WANG Hemei .
Affiliation:Department of Anesthesiology, General Hospital of People's Liberation Army, Beijing 100853, China.
Abstract:
Objective: To study the role of a protease inhibitor(ulinastatin) in protection of lung damage following hepatic ischemia/reperfusion in rat. Methods: Thirtytwo healthy male SD rats were randomly divided into four groups( n =8 in each group). Group A was served as shaminjury control group, group B rats were subjected to 90 minutes hepatic ischemia, group C rats underwent 120 minutes reperfusion after 90 minutes ischemia of the liver. Ulinastatin(UTI)was administered to animals in group D which were reperfused 120 minutes after 90 minutes of ischemia of the liver. In addition to plasma malondialdehyde(MDA), bronchoalveolar lavage fluid protein(BALFP) content, and lung drytowet weight ratios (D/W) were respectively examined in each group. The concentration of myeloperoxidase(MPO) in lung tissue was also measured. Results: Compared to group A, plasma MDA, content of MPO in lung tissues and BALFP were significantly increased in both group B and group C, but they were much lower than those in group D. In addition, D/W was markedly decreased during hepatic ischemia and after 120 minutes reperfusion, while it was significantly increased in animals pretreated with UTI. Conclusion: Acute lung injury after hepatic ischemia and reperfusion is mainly induced by the oxidant stress, and neutrophil infiltration in the lung tissues are responsible for the damage under these conditions. Proteases inhibitors such as UTI might have antioxidation effect which attenuate lung injury induced by trauma to remote organs.
Keywords:acute lung injury  multiple organ failure  hepatic ischemiareperfusion injury  proteases inhibitor
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