Complement-mediated lung injury and neutrophil retention after intestinal ischemia-reperfusion

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Abstract
Xiao, Feng, Michael J. Eppihimer, Bradley H. Willis, and Donna L. Carden. Complement-mediated lung injury and neutrophil retention after intestinal ischemia-reperfusion. J. Appl. Physiol. 82(5): 1459–1465, 1997.—Complement-mediated neutrophil activation appears to play an important role in ischemia-reperfusion (I/R) injury in a variety of tissues, including the heart, lung, and small bowel. The objective of this study was to determine whether inhibition of the alternative and classic complement cascades by administration of soluble complement receptor 1 (sCR1) prevents the increased neutrophil stiffness, lung neutrophil retention, and pulmonary microvascular injury elicited by a systemic inflammatory insult. Isolated lungs were perfused with blood obtained from animals subjected to 2 h of intestinal ischemia and 20 min of reperfusion (I/R) or control (nonischemic) surgery. Intestinal I/R resulted in a significant increase in neutrophil stiffness, lung neutrophil retention, and increased pulmonary microvascular permeability, effects that were prevented by administration of sCR1 before intestinal reperfusion. The results of this study suggest that I/R injury in the gut is a potent systemic inflammatory stimulus that induces complement-mediated neutrophil stiffness, lung neutrophil entrapment, and pulmonary microvascular dysfunction.