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Ann Thorac Surg 1998;65:187-192
© 1998 The Society of Thoracic Surgeons
Department of Cardiothoracic Surgery, Wythenshawe Hospital, Manchester, United Kingdom
Accepted for publication July 3, 1997.
Dr Hooper, Department of Cardiothoracic Surgery, Wythenshawe Hospital, Southmoor Rd, Manchester M23 9LT, United Kingdom.
Background. We have previously shown that an initial 10-minute period of low-pressure reperfusion prevents the lung graft dysfunction that follows physiologic-pressure reperfusion. Possible mechanisms were investigated in this study.
Methods. Rat lungs were reperfused ex vivo using a parabiotic animal after 0-hour (groups A through C) or 24-hour (groups D through G) storage. Reperfusion pressure was either physiologic (groups A through D) or reduced by 50% for a specified time (groups E through G). The duration of reperfusion was 5 minutes (groups A, D, and E), 10 minutes (groups B and F), or 30 minutes (groups C and G), at which time endothelial permeability was measured through iodine 125labeled albumin leakage and neutrophil sequestration through tissue myeloperoxidase activity.
Results. Graft function in group D deteriorated rapidly, whereas groups E through G performed at control levels. Albumin leakage was significantly elevated in group D; with controlled reperfusion, it was elevated after 5 minutes (group E) but had returned to baseline at 10 minutes (group F) and 30 minutes (group G). Myeloperoxidase levels were not significantly different between groups.
Conclusions. Endothelial permeability is transiently elevated in the early phase of lung graft reperfusion. Initial low-pressure reperfusion may be protective by preventing irreversible edema formation during this period.
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