title: Pulmonary lactate release in patients with acute lung injury is not attributable to lung tissue hypoxia.
abstract: OBJECTIVE
  To determine whether pulmonary lactate production in patients with acute lung injury is attributable to lung tissue hypoxia.
  
  
  METHODS
  Prospective, controlled, clinical study.
  
  
  METHODS
  A multidisciplinary university intensive care unit in a general hospital.
  
  
  METHODS
  Seventy consecutive critically ill patients requiring mechanical ventilation and invasive hemodynamic monitoring. Of these patients, 18 had no acute lung injury (no ALI); 33 had acute lung injury (ALI) (Lung Injury Score [LIS] < or =2.5); and 19 had acute respiratory distress syndrome (ARDS) (LIS >2.5).
  
  
  METHODS
  None.
  
  
  RESULTS
  After hemodynamic measurements, lactate and pyruvate concentrations were assessed in simultaneously drawn arterial (a) and mixed venous (v) blood samples. Pulmonary lactate release was calculated as the product of transpulmonary a-v lactate difference (L[a-v]) times the cardiac index. Two indices of anaerobic metabolism of the lung, i.e., the transpulmonary a-v difference of lactate pyruvate ratio (L/P[a-v]) and excess lactate formation across the lungs (XL), were calculated. L(a-v) and pulmonary lactate release were higher in patients with ARDS than in the other groups (p<.001), and they were also higher in patients with ALI compared with patients with no ALI (p<.001). In patients with ALI and ARDS (n = 52), pulmonary lactate release correlated significantly with LIS (r2 = .14, p<.01) and venous admixture (r2 = .13, p<.01). When all patients were lumped together (n = 70), pulmonary lactate release directly correlated with LIS (r2 = .30, p<.001), venous admixture (r2 = .26, p<.001), and P(A-a)O2 (r2 = .14, p<.01). Neither L/P(a-v) nor XL was significantly different among the three groups.
  
  
  CONCLUSIONS
  The lungs of patients with ALI produce lactate that is proportional to the severity of lung injury. This lactate production does not seem to be attributable to lung tissue hypoxia.
authors.affiliation: Department of Critical Care and Pulmonary Services, Medical School of Athens University, Evangelismos Hospital, Greece.
authors.forename: C
authors.initials: C
authors.lastname: Routsi
authors.forename: H
authors.initials: H
authors.lastname: Bardouniotou
authors.forename: V
authors.initials: V
authors.lastname: Delivoria-Ioannidou
authors.forename: D
authors.initials: D
authors.lastname: Kazi
authors.forename: C
authors.initials: C
authors.lastname: Roussos
authors.forename: S
authors.initials: S
authors.lastname: Zakynthinos
mesh_terms: D015415:Biomarkers / Q000097:blood; D015687:Cell Hypoxia; D006439:Hemodynamics; D006801:Humans; D019344:Lactic Acid / Q000097:blood*; D008168:Lung / Q000378:metabolism*; D008875:Middle Aged; D011446:Prospective Studies; D019289:Pyruvic Acid / Q000097:blood; D012121:Respiration, Artificial; D012124:Respiratory Care Units; D012128:Respiratory Distress Syndrome / Q000097:blood* / Q000503:physiopathology / Q000628:therapy; D012720:Severity of Illness Index
chemical_list: D015415:Biomarkers; D019344:Lactic Acid; D019289:Pyruvic Acid