gms | German Medical Science

20. Jahrestagung der Deutschen Gesellschaft für Thoraxchirurgie

Deutsche Gesellschaft für Thoraxchirurgie

22.09. bis 24.09.2011, Düsseldorf-Kaiserswerth

Impact of an oxygen scavenger and NF-κB-inhibitor (amifostine) on acute ischemia-reperfusion injury of the lung in an in-vivo animal model

Meeting Abstract

  • B. Danner - Universitätsmedizin Göttingen, Thorax-, Herz- und Gefäßchirurgie, Göttingen
  • A. Emmert - Universitätsmedizin Göttingen, Thorax-, Herz- und Gefäßchirurgie, Göttingen
  • Ph. Klumpen - Universitätsmedizin Göttingen, Thorax-, Herz- und Gefäßchirurgie, Göttingen
  • J. Emmigholz - Universitätsmedizin Göttingen, Thorax-, Herz- und Gefäßchirurgie, Göttingen
  • V. Didilis - Universitätsmedizin Göttingen, Thorax-, Herz- und Gefäßchirurgie, Göttingen
  • R. Waldmann-Beushausen - Universitätsmedizin Göttingen, Thorax-, Herz- und Gefäßchirurgie, Göttingen
  • C. Mühlfeld - Justus-Liebig Universität Gießen, Institut für Anatomie und Zellbiologie, Gießen
  • F. Schöndube - Universitätsmedizin Göttingen, Thorax-, Herz- und Gefäßchirurgie, Göttingen

Deutsche Gesellschaft für Thoraxchirurgie. 20. Jahrestagung der Deutschen Gesellschaft für Thoraxchirurgie. Düsseldorf, 22.-24.09.2011. Düsseldorf: German Medical Science GMS Publishing House; 2011. DocHS 7.6

DOI: 10.3205/11dgt10, URN: urn:nbn:de:0183-11dgt102

Veröffentlicht: 19. September 2011

© 2011 Danner et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Objective: Ischemia-reperfusion injury (IRI) is a common problem in cardiothoracic surgery. We hypothesized that amifostine reduces pulmonary edema (PE) formation and blood-air barrier damage as well as the activation of NF-ĸB in IRI of the lung.

Methods: In male Wistar rats (n=69) a tracheotomy for controlled ventilation and a median sternotomy was performed. For induction of lung injury either the complete left hilum or selectively the left pulmonary artery was clamped for 60 minutes with a reperfusion time of 90 minutes thereafter. NaCl or amifostine (100 mg/kg) was administered either as single dose one hour before ischemia or as double dose additionally after ischemia. Blood samples from both atria and lung tissue for electron microscopy (EM) were collected at the end of the study.

Results: In EM the blood-air barrier of the lung was equally destroyed in all groups, independently of amifostine application. The PE was slightly reduced after amifostine medication when complete clamping of the hilum was performed (0.11 versus 0.045%, p=0.06). Levels of cytokines IL-6, IL-10 and IL-1β were significantly decreased after application of double dose of amifostine only in the setting of complete clamping of the hilum (833 versus 61, 530 versus 99, and 180 versus 22 pg*ml-1, p<0.005, respectively). NF-ĸB levels were not modified.

Conclusion: Amifostine had a slightly effect on intraalveolar edema and in total ischemia a significant reduction on inflammation markers was marked, whereas NF-?B was not influenced. Damage of blood-air barrier in EM is equally disastrous independently to amifostine medication.