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Ann Thorac Surg 1991;51:573-578
© 1991 The Society of Thoracic Surgeons
a Department of Cardiothoracic Surgery, Ren Ji Hospital, Shanghai Second Medical University, Shanghai, China
b Department of Cardiopulmonary Surgery, Research Division, University Hospital, Groningen, The Netherlands
Accepted for publication October 23, 1990.
* Address reprint requests to Dr Wildevuur, Department of Cardiopulmonary Surgery, Research Division, University Hospital Groningen, 59 Oostersingel, 9713 EZ Groningen, The Netherlands.
The effect of blood activation on lung reperfusion injury during cardiopulmonary bypass was investigated in 20 dogs with the use of a bubble oxygenator (n = 10) or a membrane oxygenator (n = 10). In the bubble oxygenator group, significant leukocyte and platelet right to left atrium gradients were found 15 minutes after lung reperfusion (p < 0.05, p < 0.01) accompanied by a sharp increase in plasma malondialdehyde concentration 5 minutes after lung reperfusion, whereas no significant right to left atrium gradient of leukocytes or platelets nor significant increase in plasma malondialdehyde concentration was observed in the membrane oxygenator group. In both the bubble oxygenator and membrane oxygenator group, similar mild to moderate lung histological changes were found before lung reperfusion. After lung reperfusion, however, more endothelial cell swelling (p < 0.05), leukocyte (p < 0.01) and platelet (p < 0.01) accumulation in lung capillaries, leakage of erythrocytes into the alveolar space (p < 0.05), and type I cell damage (p < 0.05) were found only in the bubble oxygenator group. Eventually, a significantly higher lung water content was found in the bubble oxygenator group than in the membrane oxygenator group (p < 0.01) after cardiopulmonary bypass. This study indicated that lung injury during cardiopulmonary bypass starts mainly after lung reperfusion, which was correlated with lung leukocyte and platelet sequestration associated with different types of oxygenators.
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