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Thomas M. Egan
Paola Ciriaco
Andy Kiser
John Sadoff
Mark Bleiweis
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Right arrow Lung - transplantation

Ann Thorac Surg 2004;77:1048-1055
© 2004 The Society of Thoracic Surgeons

Original article: general thoracic

Trigger for intercellular adhesion molecule-1 expression in rat lungs transplanted from non–heart-beating donors

Thomas M. Egan, MDa*, Yalaunda Thomas, MDa, Debra Gibson, MDa, William Funkhouser, MD, PhDa, Paola Ciriaco, MDb, Andy Kiser, MDa, John Sadoff, MDa, Mark Bleiweis, MDa, Clarence E. Davis, PhDa

a University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
b San Raffaele Hospital, University of Milan, Milan, Italy

Accepted for publication August 28, 2003.

* Address reprint requests to Dr Egan, University of North Carolina at Chapel Hill, Medical School Wing C-Room 354, CB 7065, Chapel Hill, NC 27599-7065, USA.
e-mail: ltxtme{at}med.unc.edu

Presented at the Thirty-ninth Annual Meeting of The Society of Thoracic Surgeons, San Diego, CA, Jan 31–Feb 2, 2003.

BACKGROUND: Lung transplantation from non–heart-beating donors causes ischemia-reperfusion injury. We sought to determine the trigger for expression of intercellular adhesion molecule-1 (ICAM-1) caused by ischemia-reperfusion injury.

METHODS: Thirty-six Sprague-Dawley rats underwent left lung transplant (six groups of 6). Lungs were transplanted immediately after arrest, or from non–heart-beating donors after 2 hours of oxygen-ventilation or no ventilation. Recipients were reperfused for 4 or 6 hours, then lungs were stained with a mouse anti-rat ICAM-1 monoclonal antibody, developed with avidin-biotin peroxidase to a biotinylated anti-mouse immunoglobin G antibody. Intercellular adhesion molecule-1 expression was graded by two masked observers as 0 = absent, 1 = weak, or 2 = strong in alveoli, arterioles, and venules. Explanted recipient left lungs served as negative controls, and positive controls were generated 6 hours after intraperitoneal injection of endotoxin. Intercellular adhesion molecule-1 expression above baseline among groups was compared by Fisher's exact test.

RESULTS: Constitutive expression of ICAM-1 was present in rat lung alveoli, with 24 of 35 controls staining weakly and 4 of 35 strongly positive in alveolar areas. Intercellular adhesion molecule-1 expression was not increased in transplanted lungs evaluated after 4 hours of reperfusion, even lungs retrieved from non–heart-beating donors. But when non–heart-beating donor lungs were assessed 6 hours after onset of reperfusion, ICAM-1 expression was significantly more apparent in alveolar and arteriolar areas, compared with controls and lungs transplanted immediately after arrest.

CONCLUSIONS: Lungs transplanted immediately after circulatory arrest do not sustain sufficient ischemia-reperfusion injury to upregulate ICAM-1. Onset of reperfusion is the signal for ICAM-1 expression, not the onset of ischemia or the total duration of ischemic and reperfusion time together. Strategies at reperfusion may minimize ICAM-1 expression.




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