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(American Journal of Pathology. 2004;164:2241-2249.)
© 2004 American Society for Investigative Pathology

Up-Regulation of Endothelial Nitric Oxide Synthase Inhibits Pulmonary Leukocyte Migration Following Lung Ischemia-Reperfusion in Mice

Alexander Kaminski*, Christiane Backhaus Pohl*, Christoph Sponholz*, Nan Ma*, Christof Stamm*, Brigitte Vollmar{dagger} and Gustav Steinhoff{dagger}

From the Department of Cardiac Surgery*and the Department of Experimental Surgery,{dagger}University of Rostock, Rostock, Germany

Endogenous nitric oxide (NO) is known to modulate post-ischemic inflammatory response in various organs. However, the role of nitric oxide synthase isoforms (NOS) in mediating pulmonary post-ischemic inflammatory response is poorly understood. We therefore studied post-ischemic endothelial adhesion molecule expression and leukocyte migration in endothelial NOS knockout (eNOS-KO) mice subjected to pulmonary ischemia and reperfusion in vivo. Under anesthesia and mechanical ventilation, the left pulmonary hilum in wild-type (WT) and eNOS-KO mice was clamped for 1 hour, followed by reperfusion for up to 24 hours. In WT mice, we observed a selective up-regulation of both eNOS mRNA and protein in lung tissue, while inducible NOS (iNOS) and neuronal NOS (nNOS) remained unchanged. Survival in eNOS-KO mice was reduced due to severe pulmonary edema, underlining an increased susceptibility to ischemia-reperfusion (I/R) injury. Interstitial tissue infiltration by CD18- and CD11a-positive white blood cells as well as lung tissue water content peaked at 5 hours of reperfusion and were found significantly higher than in WT mice. Enhanced leukocyte-endothelial interaction was associated with pronounced up-regulation of vascular cell adhesion molecule (VCAM) in eNOS-KO mice during post-ischemic reperfusion. We conclude that eNOS attenuates post-ischemic inflammatory injury to the lung most probably via inhibition of endothelial adhesion molecule expression.




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