Release of lactate by the lung in acute lung injury

The pathogenesis of hyperlactatemia during sepsis is poorly understood. We have previously described an increase in lactate concentration across the lung in the dog during early endotoxemia. Accordingly, we sought to determine if the lung releases lactate in humans and what relation this has with lung injury. Methods: We measured lactate concentrations across the lung and lung injury scores (LIS) in two groups of patients. Group 1 consisted of nine patients with acute lung injury (LIS greater than or equal to 2.0) and elevated lactate concentrations (>2.0 mmol/L). Group 2 contained 12 patients with no acute lung injury (LIS scores less than or equal to 1.5), with or without increased lactate concentrations. Simultaneous measurements of plasma lactate and blood gases were obtained from indwelling arterial and pulmonary artery catheters. Measurements of cardiac output were also obtained. Lactate measurements were done using a lactate analyzer (PSI; Fellow Springs, Ohio). Results: For each patient with acute lung injury and hyperlactatemia, an arterial-venous lactate gradient existed demonstrating release of lactate by the lung. This gradient persisted after correction for changes in hemoconcentration across the lung. The mean lactate gradient across the lung was 0.4+/-0.2 mmol/L for group 1 vs 0.05+/-0.1 mmol/L for group 2 (p=0.001). This corresponded to a mean pulmonary lactate flux of 231.3+/-211.3 vs 5.0+/-37.2 mmol/h (p=0.001). The lactate flux and the arterial-venous lactate difference correlated with LIS both for the entire sample and for the subgroup with hyperlactatemia (r=0.69, p<0.01). Pulmonary lactate Ru was not related to arterial lactate levels (r=0.25). Conclusion: In patients with acute lung injury and hyperlactatemia, the lung is a major source of lactate and lactate flux correlates with LIS. This lactate flux could explain some of the hyperlactatemia seen in sepsis.