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Am J Physiol Lung Cell Mol Physiol 279: L528-L536, 2000;
1040-0605/00 $5.00
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Vol. 279, Issue 3, L528-L536, September 2000

Attenuation of lung reperfusion injury after transplantation using an inhibitor of nuclear factor-kappa B

Scott D. Ross1, Irving L. Kron1, James J. Gangemi1, Kimberly S. Shockey1, Mark Stoler2, John A. Kern1, Curtis G. Tribble1, and Victor E. Laubach1

Departments of 1 Surgery and 2 Pathology, University of Virginia Health Sciences Center, Charlottesville, Virginia 22908

A central role for nuclear factor-kappa B (NF-kappa B) in the induction of lung inflammatory injury is emerging. We hypothesized that NF-kappa B is a critical early regulator of the inflammatory response in lung ischemia-reperfusion injury, and inhibition of NF-kappa B activation reduces this injury and improves pulmonary graft function. With use of a porcine transplantation model, left lungs were harvested and stored in cold Euro-Collins preservation solution for 6 h before transplantation. Activation of NF-kappa B occurred 30 min and 1 h after transplant and declined to near baseline levels after 4 h. Pyrrolidine dithiocarbamate (PDTC), a potent inhibitor of NF-kappa B, given to the lung graft during organ preservation (40 mmol/l) effectively inhibited NF-kappa B activation and significantly improved lung function. Compared with control lungs 4 h after transplant, PDTC-treated lungs displayed significantly higher oxygenation, lower PCO2, reduced mean pulmonary arterial pressure, and reduced edema and cellular infiltration. These results demonstrate that NF-kappa B is rapidly activated and is associated with poor pulmonary graft function in transplant reperfusion injury, and targeting of NF-kappa B may be a promising therapy to reduce this injury and improve lung function.

pyrrolidine dithiocarbamate; ischemia; organ preservation


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