Leukocyte and endothelial activation in a laboratory model of extracorporeal membrane oxygenation (ECMO)

An inflammatory response and a capillary leak syndrome frequently develop d uring the treatment of neonatal respiratory failure by extracorporeal membr ane oxygenation (ECMO). The present study was performed to investigate leuk ocyte activation and endothelial cell dysfunction that are associated with prolonged contact of blood components with synthetic surfaces. Laboratory E CMO was performed with fresh human blood at 37 degreesC for 8 h (n = 6), Le ukocyte activation was measured by L-selectin (CD62L) and CD18 integrin sur face expression and by neutrophil-derived elastase release. To monitor endo thelial activation, endothelial cell ICAM-1 (CD54) expression was measured in cultured endothelial cells from human umbilical veins (HUVEC) after incu bation with plasma from the ECMO experiments. CD18 integrin expression was found significantly upregulated on polymorphonuclear neutrophils and monocy tes after 2-4 h of laboratory ECMO. L-selectin was reduced on both cell typ es during the total duration of the experiments. Soluble L-selectin (sCD62L ) and total and differential leukocyte counts remained unchanged during the experiment. Neutrophil-derived elastase content was maximal after 8 h of E CMO. Plasma from the ECMO experiments did not induce ICAM-1 expression of c ultured HUVEC. We conclude that prolonged contact with synthetic surfaces d uring ECMO activates phagocytes, which may contribute to the inflammatory r esponse seen in ECMO-treated patients. Activated phagocytes do not accumula te in the extracorporeal system nor release humoral factors inducing ICAM-1 expression on endothelial cells.