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The histological changes of oleic acid lung injury are associated with marked functional changes. Pulmonary microvascular permeability is markedly increased, with elevation of extravascular lung water and leakage of protein-rich fluid into the interstitium and the air spaces (46, 247). These changes in alveolar permeability are proportional to the dose of oleic acid, develop within 1 h of administration, and are rapidly reversible, with the alveolar fluid clearance normalizing within 8 h (54). There are also severe alterations in gas exchange, with respiratory acidosis, hypoxemia, and increased alveolar-arterial oxygen difference within 90 min of intravenous administration (40, 46, 170, 221). The gas exchange alterations result from severe ventilation/perfusion (V/Q) mismatching, increased intrapulmonary shunt, and increased dead space ventilation (170). The static lung compliance and functional residual capacity (FRC) fall rapidly, and mean airway pressure rises (40, 125). Systemically, the cellular damage induced by oleic acid becomes evident rapidly, and increases in circulating angiotensin converting enzyme (ACE) can be detected within 2.5 min after intravenous administration of 0.1 ml/kg to dogs (151). The hemodynamic responses are dose dependent and are characterized by myocardial depression, early systemic hypotension, and pulmonary hypertension (40, 46, 125, 190, 231).