COMPLEMENT-MEDIATED LUNG INJURY AND NEUTROPHIL RETENTION AFTER INTESTINAL ISCHEMIA-REPERFUSION

Complement-mediated neutrophil activation appears to play an important role in ischemia-reperfusion (I/R) injury in a variety of tissues, in cluding the heart, lung, and small bowel. The objective of this study was to determine whether inhibition of the alternative and classic com plement cascades by administration of soluble complement receptor 1 (s CR1) prevents the increased neutrophil stiffness, lung neutrophil rete ntion, and pulmonary microvascular injury elicited by a systemic infla mmatory insult. Isolated lungs were perfused with blood obtained from animals subjected to 2 h of intestinal ischemia and 20 min of reperfus ion (I/R) or control (nonischemic) surgery. Intestinal YR resulted in a significant increase in neutrophil stiffness, lung neutrophil retent ion, 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 po tent systemic inflammatory stimulus that induces complement-mediated n eutrophil stiffness, lung neutrophil entrapment, and pulmonary microva scular dysfunction.