Pathophysiology of ovine smoke inhalation injury treated with extracorporeal membrane oxygenation

• Published in: Chest Vol. 103; no. 5; p. 1582
• Main Authors: Zwischenberger, J B, Cox, Jr, C S, Minifee, P K, Traber, D L, Traber, L D, Flynn, J T, Linares, H A, Herndon, D N
• Format: Journal Article
• Language: English
• Published: United States 01.05.1993
• Subjects: Animals; Cardiac Output; Extracorporeal Membrane Oxygenation - methods; Female; Free Radicals; Hemodynamics; Leukocyte Count; Oxygen - metabolism; Pulmonary Gas Exchange; Sheep; Smoke Inhalation Injury - physiopathology; Smoke Inhalation Injury - therapy; Thromboxane B2 - blood
• ISSN: 0012-3692; 1931-3543
• DOI: 10.1378/chest.103.5.1582

An ovine model was used to study the pathophysiology of smoke inhalation injury treated with extracorporeal membrane oxygenation (ECMO). Smoke inhalation is characterized by leukocyte-oxygen free-radical mediated acute lung injury. Treatment with ECMO was by extracorporeal venoarterial or venovenous perfusion using a venous drainage reservoir, roller pump, heat exchanger, and membrane lung oxygenator capable of oxygen delivery to and carbon dioxide removal from a patient. Blood-foreign surface interactions are known to occur during ECMO. We examined the effects of ECMO on circulating leukocytes, oxygen free-radical activity, thromboxane release, and gas exchange after smoke inhalation injury. Animals treated with smoke and ECMO had significantly increased circulating thromboxane B2 levels and oxygen free-radical activity compared with sham-treated animals and animals treated with smoke and mechanical ventilation (MV). Likewise, there was a significant increase in lung wet-to-dry weight ratios in animals treated with smoke and ECMO compared with those treated with smoke and MV. These data may account for the initial deterioration in native lung function after the initiation of ECMO and imply that ECMO may potentiate the pathophysiology of smoke inhalation injury.