title: Effects of a catecholamine-induced increase in cardiac output on lung injury after experimental unilateral pulmonary acid instillation.
abstract: OBJECTIVE
  Increasing pulmonary blood flow aggravated ventilation-associated lung injury in ex vivo animal experiments, but data were less consistent in an in vivo animal model and do not reflect redistributed lung perfusion seen in clinical acute lung injury. We sought to determine the effects of increased cardiac output on markers of lung injury in an in vivo model of inhomogeneous lung perfusion and injury.
  
  
  METHODS
  Prospective, controlled animal study.
  
  
  METHODS
  Experimental research laboratory of a university hospital.
  
  
  METHODS
  A total of 50 anesthetized, mechanically ventilated, male Wistar rats.
  
  
  METHODS
  Unilateral lung injury was induced in rats by left lung acid instillation. After 24 hrs, animals were anesthetized and subjected to mechanical ventilation (tidal volume, 8 mL/kg; positive end-expiratory pressure, 7 cm H2O; FIO2, 0.4) and continuous infusion of either 10 microg x kg x min dobutamine or isotonic saline (control) for 4 hrs.
  
  
  RESULTS
  Cardiac output and differential lung perfusion were recorded throughout the ventilation period. Right and left lung wet-to-dry weight ratio, cytokines and inflammatory cells in lung lavage, and histologic lung injury were measured postmortem. After acid injury, lung perfusion was preferentially distributed to the noninjured lung. Dobutamine increased baseline cardiac output (>70%) and perfusion of both lungs (left, acid-instilled lung: from 16 +/- 2 to 29 +/- 6 mL/min; right, non-acid-instilled lung: from 54 +/- 3 to 98 +/- 7 mL/min). There was no difference in left lung injury between dobutamine- and saline-infused animals, but right lung injury was aggravated in dobutamine-infused animals, as indicated by increased lung edema, histologic lung injury, and cell counts in lavage.
  
  
  CONCLUSIONS
  In the setting of unilateral lung injury and uneven lung perfusion, a dobutamine-induced increase in cardiac output has potentially detrimental effects on the opposite lung.
authors.affiliation: Department of Anesthesiology and Intensive Care Medicine, Friedrich-Schiller-Universität Jena, Jena, Germany. torsten.schreiber@med.uni-jena.de
authors.forename: Torsten
authors.initials: T
authors.lastname: Schreiber
authors.forename: Lars
authors.initials: L
authors.lastname: Hueter
authors.forename: Elke
authors.initials: E
authors.lastname: Gaser
authors.forename: Barbara
authors.initials: B
authors.lastname: Schmidt
authors.forename: Konrad
authors.initials: K
authors.lastname: Schwarzkopf
authors.forename: Waheedullah
authors.initials: W
authors.lastname: Karzai
mesh_terms: D000818:Animals; D002302:Cardiac Output; D002316:Cardiotonic Agents / Q000009:adverse effects*; D016207:Cytokines / Q000187:drug effects / Q000378:metabolism; D004195:Disease Models, Animal; D004280:Dobutamine / Q000009:adverse effects*; D008168:Lung / Q000098:blood supply* / Q000187:drug effects / Q000473:pathology; D008297:Male; D008863:Microspheres; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D012121:Respiration, Artificial / Q000009:adverse effects*; D012128:Respiratory Distress Syndrome / Q000139:chemically induced / Q000209:etiology / Q000503:physiopathology*
chemical_list: D002316:Cardiotonic Agents; D016207:Cytokines; D004280:Dobutamine