Am. J. Respir. Crit. Care Med., Vol 150, No. 4, Oct 1994, 1032-1037.
Lung oxidant injury in a model of lung storage and extended reperfusion
NA Christie, DE Smith, KN Decampos, AS Slutsky, GA Patterson and AK Tanswell
Medical Research Council Group in Lung Development, Hospital for Sick Children Research Institute, Toronto, Ontario, Canada.
Donor lungs for transplantation are susceptible to "preservation" injury
during both storage and postimplantation reperfusion. We investigated
whether lung dysfunction seen after storage and reperfusion was associated
with any biochemical hallmarks of direct cellular oxidant injury to lipid,
protein, or DNA. Heart/lung blocks were extracted from adult rats following
pulmonary vascular flush. Lungs were either perfused immediately ex vivo
for 2 h with deoxygenated venous rat blood or were stored at 10 degrees C
for 13 h before perfusion. Stored lungs had increased airway pressure,
pulmonary vascular shunt fraction, wet/dry weight ratio, and parenchymal
hemorrhage after perfusion but no change in pulmonary artery pressure
compared with immediately perfused lungs. Hypothermic storage caused no
biochemical changes in lung tissue. Perfusion of fresh or stored lungs
resulted in lipid peroxidation and loss of nonprotein reduced sulfhydryls;
sulfhydryl loss was threefold higher in lungs stored before perfusion
compared with freshly perfused lungs. Reperfusion of stored, not fresh,
lungs was associated with DNA damage. No loss of protein sulfhydryls
occurred following lung perfusion. We conclude that DNA damage, loss of
reduced nonprotein sulfhydryls, and lipid peroxidation during reperfusion
of stored lungs may be responsible for physiologic lung dysfunction.
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Copyright © 1994 American Thoracic Society
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