Objective: To define the mechanisms responsible for the lung leukosequ
estration and injury elicited by intestinal ischemia/reperfusion (I/R)
. Methods: The effect of 120 minutes of superior mesenteric artery occ
lusion and 90 minutes of reperfusion on neutrophil deformability, lung
neutrophil retention, and pulmonary microvascular permeability was de
termined. Results: Compared with control surgery, intestinal I/R resul
ted in a significant increase in neutrophil stiffness (mean yield pres
sure [P-yield] 1.533 +/- 0.075 and 2.302 +/- 0.288 cm H2O, respectivel
y) and lung neutrophil content (6.3 +/- 1.4 and 31.5 +/- 6.4 U/g wet w
eight, respectively). These changes were not affected by inhibition of
neutrophil adherence before gut reperfusion. However. the increased l
ung microvascular permeability elicited by gut I/R (0.111 +/- 0.020 [c
ontrol surgery] and 0.255 +/- 0.041 [I/R] mL/min/cm H2O/100 g lung tis
sue) was significantly attenuated by administration of antibodies dire
cted against neutrophil or endothelial determinants of leukocyte adhes
ion. Conclusions: The results of this study suggest that intestinal I/
R is a potent inflammatory stimulus thar elicits an increase in neutro
phil stiffness and lung neutrophil retention independent of neutrophil
-endothelial cell adhesion. In contrast, the increased lung microvascu
lar permeability elicited by gut I/R is attenuated by strategies that
interfere with neutrophil-endothelial cell adhesion.