A Urinary Test for Pulmonary Arterial Hypertension ?

have fewer neutrophils sequestered in the pulmonary circulation, but more neutrophils in the airspaces than wild-type mice after cecal ligation and puncture (16). High Vt ventilation can induce iNOS expression and activity in the airspace, and reactive nitrogen species contribute to impaired alveolar epithelial fluid transport and pulmonary edema in VILI (17). The mechanisms of cLT-mediated lung permeability are uncertain, and how cLTs may influence NO-mediated alteration in barrier function and neutrophil trafficking remains to be investigated. Caironi and colleagues (6) have further clarified our understanding of the pathogenesis of VILI. Early events, such as mechanical disruption of the basement membrane, disruption of the plasma membrane, or mechanically triggered chemical signaling, initiate an inflammatory program that culminates in neutrophil recruitment and activation that amplifies lung injury. The effects of lipid mediators, including arachidonic acid metabolites, in the pathogenesis of VILI appear to be greater than previously recognized and should stimulate renewed interest in 5-LO inhibitors for the treatment of acute lung injury.

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