ObjectiveTo determine the length of warm ischemic tolerance in pulmonary grafts from non-heart-beating donors. Summary Background DataIf lungs could be retrieved for transplant after circulatory arrest, the shortage of donors might be significantly alleviated. Great concern, however, exists about the length of tolerable warm ischemia before cold preservation of pulmonary grafts retrieved from such non-heart-beating donors. MethodsThe authors compared the influence of an increasing postmortem interval on graft function in an isolated, room air-ventilated rabbit lung model during blood reperfusion up to 4 hours. Four groups of cadavers (four animals per group) were studied. In group 1, lungs were immediately reperfused. In the other groups, cadavers with lungs deflated were left at room temperature for 1 hour (group 2), 2 hours (group 3), or 4 hours (group 4). ResultsPulmonary vascular resistance was enhanced in all ischemic groups compared with the control group. An increase was noted with longer postmortem intervals in peak airway pressure and in weight gain. A concomitant decline was observed in the venoarterial oxygen pressure gradient caused by progressive edema formation, as reflected by the wet-to-dry weight ratio at the end of reperfusion. ConclusionsWarm ischemia resulted in increased pulmonary vascular resistance. Graft function in lungs retrieved 1 hour after death was not significantly worse than in nonischemic lungs. Therefore, 60 minutes of warm ischemia with the lung collapsed may be tolerated before cold storage. Further studies are necessary to investigate whether lungs retrieved from nonheart-beating donors will become a realistic alternative for transplant.

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These data suggest that: (1) pulmonary edema will develop in atelectatic lungs if reperfusion is delayed for 4 h after death; (2) postmortem room air-inflation is as good as ventilation in prolonging warm ischemic tolerance; (3) ventilation with room air is no different from that with nitrogen; (4) therefore, prevention of alveolar collapse appears to be the critical factor in protecting the warm ischemic lung from reperfusion injury independent of continuous oxygen supply.