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Early hemodynamic injury during donor brain death determines the severity of primary graft dysfunction after lung transplantation

Lookup NU author(s): Vassillios Avlonitis, Chris Wigfield, Dr Huw Golledge, Emeritus Professor John Kirby, Professor John Dark

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Abstract

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.

Publication metadata

Author(s): Avlonitis VS, Wigfield CH, Golledge HDR, Kirby JA, Dark JH

Publication type: Article

Publication status: Published

Journal: American Journal of Transplantation

Year: 2007

Volume: 7

Issue: 1

Pages: 83-90

ISSN (print): 1600-6135

ISSN (electronic): 1600-6143

Publisher: Wiley-Blackwell Publishing, Inc.

URL: http://dx.doi.org/10.1111/j.1600-6143.2006.01593.x

DOI: 10.1111/j.1600-6143.2006.01593.x

PubMed id: 17227559

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