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Ann Thorac Surg 1999;67:769-775
© 1999 The Society of Thoracic Surgeons
a Department of Surgery, Duke University Medical Center, Durham, North Carolina, USA
b Department of Pediatrics, Duke University Medical Center, Durham, North Carolina, USA
c Department of Immunology, Duke University Medical Center, Durham, North Carolina, USA
d Nextran, Princeton, New Jersey, USA
Accepted for publication July 15, 1998.
Address reprint requests to Dr Davis, Department of Surgery, Duke University Medical Center, PO Box 3864, Durham, NC 27710
e-mail: davis053{at}mc.duke.edu
Background. Pulmonary xenotransplantation is not possible because of hyperacute lung injury, the pathogenesis of which is unknown. This study evaluates complement-dependent pathways of pulmonary injury during heterologous perfusion of swine lungs.
Methods. Lungs from unmodified swine and swine expressing human decay-accelerating factor and human CD59 (hDAF/hCD59 swine) were perfused with either human plasma or baboon blood. Pulmonary vascular resistance and static pulmonary compliance were measured serially, and swine lung tissue were examined by light microscopy. Complement activation was assessed by serial measurements of baboon plasma C3a-desArg concentrations.
Results. Perfusion of unmodified swine lungs with human plasma and baboon blood resulted in hyperacute lung injury within minutes of perfusion. However, function was preserved in swine lungs expressing human decay-accelerating factor and human CD59. In both study groups, xenogeneic perfusion with baboon blood resulted in at least a sevenfold increase in plasma C3a-desArg levels suggesting transient activation of complement.
Conclusions. Lungs from swine expressing human decay-accelerating factor and human CD59 were resistant to injury during perfusion with human plasma and baboon blood, indicating that complement mediated some of the features of xenogeneic acute lung injury.
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