Neutrophils and neutrophil products do not mediate pulmonary hemodynamic effects of endotoxin on @entity3952 -induced XXXX .

@entity3952 @entity235 @entity1862 @entity26 @entity651 @entity1398 @entity358 @entity1576 @entity5567
Small-dose endotoxin (Etx) prevents pulmonary perfusion redistribution away from @entity358 after @entity3952 (OA)-induced injury in @entity235 , causing a significant deterioration in oxygenation. We hypothesized that small-dose Etx might mediate this effect via polymorphonuclear neutrophil (PMN) priming with release of inflammatory mediators such as platelet activating factor (PAF) or secretory phospholipase A(2) (sPLA(2)). To test this hypothesis, we administered specific inhibitors directed against each mediator and used two strategies to generate @entity1398 . PAF and sPLA(2) inhibitors were administered before OA injury, followed 2 h later by small-dose Etx (n = 4 each group). PMN depletion was achieved by @entity1862 administration for 5 days before the study to achieve absolute neutrophil counts <1000/mm(3) (n = 4). Inhibition of PMN adherence to lung endothelium was achieved by the administration of an anti-CD18 monoclonal antibody immediately before @entity651 (n = 5). Positron emission tomography was used to evaluate pulmonary perfusion distribution and lung water content. We observed no effect of these interventions on the perfusion pattern after Etx + OA. Thus, neither neutrophils nor @entity5567 or sPLA(2) mediate the effects of Etx on the pattern of perfusion in this model of @entity651 . IMPLICATIONS: Acute @entity1576 is characterized by severe decreases in blood @entity26 . The pattern of blood flow within the lungs can contribute to this problem. This study investigated the potential role of white blood cells and their products in mediating abnormal pulmonary blood flow patterns in an experimental animal model of @entity1576 .
