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无泵驱动体外膜肺转流治疗急性呼吸衰竭犬过程中血浆和肺组织ET-1、TNF-α水平的变化

Changes of ET-1 and TNF-α in dog ARF model during bilateral femoral arteriovenous shunt for extracorporeal membrane oxygenation
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摘要 目的观察双侧股动脉-股静脉无泵驱动体外膜肺(bAV-ECMO)治疗急性呼吸衰竭(ARF)犬过程中血浆和肺组织肿瘤坏死因子-α(TNF-α)和内皮素-1(ET-1)的变化。方法10只犬在建立ARF模型情况下给予bAV-ECMO治疗。分别于实验各时段提取肺组织及血浆,应用放射免疫技术检测TNF-α、ET-1的变化。结果模型动物血浆ET-1含量先降低,1 h后开始回升,2 h达到高值;肺组织匀浆ET-1含量增加在转流2 h达到高值。方差分析表明匀浆和血浆各自ET-1的均数在转流前后有显著性差异(P<0.05)。肺组织匀浆和血浆TNF-α含量转流3 h后均较术前有所增高,但都呈现出先降低后升高的趋势。方差分析表明匀浆和血浆中各自TNF-α的均数在转流前后有显著性差异(P<0.05)。结论bAV-ECMO早期转流可能减少ET-1的释放;而TNF-α在转流早期对于ET-1释放影响不大。 Objective To study the changes of endothelin-1(ET-1) and tumor necrosis factor alpha(TNFα ) in lung homogenate and plasm when acute respiratory failure (ARF) animal models are treated by bilateral femoral arteriovenous extracorporeal membrane oxygenation(bAV-ECMO). Methods Ten ARF dog models were treated by the bAV-ECMO. Right atrium blood and lung tissues were collected at different time points, and ET-1 and TNFα were assayed by radioimmunological method. Results ET-1 content in plasm decreased at first, and at 1 h it was elevated and at 2 h reached the peak. ET-1 content in lung homogenate reached the peak at 2 h and then started to decrease. The analysis of variance showed notable differences(P〈0.05). TNFα content in lung homogenate and plasm decreased at 1 h and started to increase after that time; it was higher at 3 h than that at the beginning of operation and increased continuously. The analysis of variance showed notable differences (P〈0.05). Conclusion Early bAV-ECMO can possibly reduce the release of ET-1, while TNFα has no obvious effect on ET-1 release during bAV-ECMO.
作者 闫炀 耿希刚
出处 《西安交通大学学报(医学版)》 CAS CSCD 北大核心 2007年第1期54-56,共3页 Journal of Xi’an Jiaotong University(Medical Sciences)
关键词 急性呼吸衰竭 内皮素-1 肿瘤坏死因子α 无泵驱动体外膜肺 acute respiratory failure(ARF) endothelin-l(ET-1) tumor necrosis factor alpha(TNFα ) extracorporeal membrane oxygenation
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参考文献3

  • 1Ichiba S,Bartlett RH.Current status of extracorporeal membrane oxygenation for severe respiratory failure[J].Artif Organs,1996,20(2):120-123.
  • 2Agani FH,Pichiule P,Chavez JC,et al.The role of mitochondria in the regulation of hypoxia inducible factor 1 expression during hypoxia[J].J Biol Chem,2000,275(3):35863-35867.
  • 3Hu J,Discher DJ,Bishopric NH,et al.Hypoxia regulates expression of the endothelin-1 gene through aproximal hypoxia in ducible factor 1 binding site on the antisense strand[J].Biochem Biophys Res Commun,1998,245(2):894-899.

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