Superoxide anion mediates pulmonary vascular permeability caused by neutrophils in cardiopulmonary bypass

During cardiopulmonary bypass (CPB), neutrophils (PMNs) may be stimulated b y shear stress which could contribute to the pulmonary injury that occurs a fter CPB. To elucidate whether mechanically stimulated PMNs increase pulmon ary vascular permeability, measured as the pulmonary filtration coefficient (K) and pulmonary vascular resistance, and to elucidate whether superoxide anion mediates this increase, we assessed the effects of stimulated and un stimulated PMNs, and of superoxide dismutase (SOD) on K and resistance in i solated perfused lungs from Sprague-Dawley rats. PMNs were stimulated by ge ntle agitation in a glass vial for 10s. Lungs perfused with the stimulated PMNs, being the stimulated group (n = 6), elicited a 5-fold increase in the filtration coefficient compared with lungs perfused with unstimulated cell s, being the unstimulated group (n = 6), This increase in filtration was co mpletely blocked by the preincubation of stimulated PMNs with CD18 monoclon al antibody, being the Ab group (n = 6), and also by superoxide dismutase, being the SOD group (n = 6). Pulmonary vascular resistance was not increase d by stimulated PMNs, and the accumulation of stimulated PMNs was not block ed by SOD. These findings suggest that stimulated PMNs increase K and that superoxide anion may injure the pulmonary vascular endothelial cells.