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Complement Inhibition Attenuates Human Lung Transplant Reperfusion Injury*: A Multicenter Trial

Martin R. Zamora, MD, FCCP; R. D. Davis, MD, FCCP; S. H. Keshavjee, MD, FCCP; L. Schulman; J. Levin; U. Ryan; G. A. Patterson, MD, FCCP
Author and Funding Information

*From the University of Colorado, Denver, CO; Duke University, Durham, NC; University of Toronto, Toronto, Ontario, Canada; Columbia-Presbyterian, New York, NY; T Cell Sciences, Needham, MA; and Washington University, St. Louis, MO.

Correspondence to: Martin R. Zamora, MD, FCCP, Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center, 4200 E Ninth Ave, Denver, CO 80262



Chest. 1999;116(suppl_1):46S. doi:10.1378/chest.116.suppl_1.46S
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Extract

Lung dysfunction due to ischemia and reperfusion (I/R) injury is a major cause of morbidity, mortality, and increased cost following human lung transplantation (LTx). Since complement (C) activation plays a significant role in I/R injury, we hypothesized that C inhibition would attenuate the degree of I/R injury following LTx. TP10 (soluble C receptor 1 inhibitor) inhibits C activation by inactivating C3 and C5 convertases.


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