Review

Leukocyte Depletion as a Mechanism for Reducing Neutrophil-Mediated Ischemic-Reperfusion Injury during Transplantation

Medical University of South Carolina, Charleston, South Carolina

^* Address correspondence to: Alicia Sievert, MS, University of California Los Angeles Medical Center, 10833 LeConte, Los Angeles, CA 90095, E-mail: aliciasievert@hotmail.com

Received: 22 March 2002
Accepted: 21 January 2003

Abstract

Patients undergoing transplantation are at high risk for leukocyte-mediated morbidity because of activated neutrophils and oxygen free radicals. This type of injury is most prominent during the reperfusion stage of transplantation. When tissue becomes ischemic, normal oxidation is altered (2). As oxygen is reintroduced to the system, oxygen free radical formation occurs via the oxidation of hypoxanthine by xanthine oxidase, causing destruction of the endothelium, increased permeability, and decreased organ function (2). In addition, neutrophils that may have already been activated by contact activation from the cardiopulmonary bypass circuit, accumulate in the ischemic organ at reperfusion (9,10). Activated neutrophils then release oxygen metabolites and proteolytic enzymes, which further destroy the integrity of the vascular endothelium (11). This insult can cause edema, capillary plugging, and poor graft function (12). Recent attempts have been made to decrease the mediators of ischemic-reperfusion injury. Perhaps the most advantageous of these attempts is the removal of leukocytes during reperfusion. This has been successfully achieved using leukocyte-depleting filters before exposing the organ to systemic blood flow (14). This article is a review of ischemic-reperfusion injury and the use of leukocyte depletion during reperfusion of transplanted organs.