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Lookup NU author(s): Vassillios Avlonitis,
Dr Huw Golledge,
Professor John Kirby,
Professor John Dark
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Sympathetic discharge and hypertensive crisis often accompany brain death, causing neurogenic pulmonary edema. Progressive systemic inflammatory response develops, which can injure the lung further. We investigated whether (a) early hemodynamic injury during donor brain death increases reperfusion injury after lung transplantation and (b) delaying lung recovery would augment reperfusion injury further, because of the progressive systemic inflammatory response in the donor. Brain death was induced by intracranial balloon inflation in rats, with or without α-adrenergic blockade pretreatment to prevent the hypertensive crisis. Another group of rats had a sham procedure. Lungs were retrieved 15 min after brain death or sham procedure and reperfused using recipient rats. In a fourth group, brain death was induced and the lungs were retrieved 5 h after brain death and reperfused. Postreperfusion, lungs retrieved early from untreated brain-dead donors developed more severe reperfusion injury, as assessed by functional parameters and inflammatory markers, than those from sham or alpha-blockade-treated donors. Lungs retrieved late from brain-dead donors had similar inflammatory markers after reperfusion to those retrieved early, but significantly lower pulmonary vascular resistance. Early hemodynamic damage during donor brain death increases reperfusion injury after lung transplantation. Delaying retrieval may allow the lung to recover from the hemodynamic injury. © 2006 The Authors.
Author(s): Avlonitis VS, Wigfield CH, Golledge HDR, Kirby JA, Dark JH
Publication type: Article
Publication status: Published
Journal: American Journal of Transplantation
ISSN (print): 1600-6135
ISSN (electronic): 1600-6143
Publisher: Wiley-Blackwell Publishing, Inc.
PubMed id: 17227559
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