Artikel
Impact of an oxygen scavenger and NF-κB-inhibitor (amifostine) on acute ischemia-reperfusion injury of the lung in an in-vivo animal model
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Autoren
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B. Danner
- Universitätsmedizin Göttingen, Thorax-, Herz- und Gefäßchirurgie, Göttingen
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A. Emmert
- Universitätsmedizin Göttingen, Thorax-, Herz- und Gefäßchirurgie, Göttingen
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Ph. Klumpen
- Universitätsmedizin Göttingen, Thorax-, Herz- und Gefäßchirurgie, Göttingen
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J. Emmigholz
- Universitätsmedizin Göttingen, Thorax-, Herz- und Gefäßchirurgie, Göttingen
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V. Didilis
- Universitätsmedizin Göttingen, Thorax-, Herz- und Gefäßchirurgie, Göttingen
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R. Waldmann-Beushausen
- Universitätsmedizin Göttingen, Thorax-, Herz- und Gefäßchirurgie, Göttingen
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C. Mühlfeld
- Justus-Liebig Universität Gießen, Institut für Anatomie und Zellbiologie, Gießen
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F. Schöndube
- Universitätsmedizin Göttingen, Thorax-, Herz- und Gefäßchirurgie, Göttingen
| Veröffentlicht: | 19. September 2011 |
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Gliederung
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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.
