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Departments of Medicine and Physiology and Biophysics, Louisiana State University Medical Center, Shreveport, Louisiana 71130
Received 18 February 1996; accepted in final form 3 January 1997.
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.
complement activation; acute respiratory distress syndrome; pulmonary capillary filtration coefficient; neutrophil deformability
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