Septic Lung

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Abstract
“Septic lung” is a variant of the acute respiratory distress syndrome. The key alterations of this syndrome are an increase in pulmonary vascular resistance and a diffuse increase in pulmonary vascular permeability, with subsequent formation of protein-rich interstitial and intraalveolar edema, disturbance of alveolar surfactant function, and severe impairment of gas exchange. In a model of blood-free perfused rabbit lungs, all these alterations in pulmonary physiology are mimicked by stimulation of the pulmonary vascular arachidonic acid (AA) cascade: increased pulmonary artery pressure is predominantly caused by the AA cyclooxygenase product thromboxane A2, whereas vascular leakage must be ascribed to the stimulation of the various AA lipoxygenase pathways. This local lipid-mediator system in the pulmonary vasculature is directly triggered by bacterial protein toxins such as Staphylococcus aureus a toxin and Pseudomonas aeruginosa cytotoxin, which start the AA cascade by serving as nonphysiologic calcium-bypass gates in cellular membranes. Moreover, bacteremia and endotoxemia may be effective via activation of the classical humoral cascade systems and leukocyte stimulation, which are all linked to the AA cascade in the pulmonary circulation as a common final pathway.

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