title: Alveolar expansion itself but not continuous oxygen supply enhances postmortem preservation of pulmonary grafts.
abstract: OBJECTIVE
  If lungs could be retrieved for transplant after circulatory arrest, the shortage of donors might be significantly alleviated. Great controversy still exists concerning the optimal mode of preservation of pulmonary grafts in these non-heart-beating donors.
  
  
  METHODS
  Graft function was measured in an isolated room air-ventilated rabbit lung model during reperfusion with homologous, diluted (Hb +/- 8.0 g/dl) and deoxygenated (PaO2 +/- 40 mmHg) blood up to 4 h. Five groups of cadavers (n = 4 in each group) were studied: In the control group, lungs were immediately reperfused. In the other groups, cadavers were left at room temperature for 4 h after death with lungs either deflated (group 1), inflated with room air (group 2), or ventilated with room air (group 3) or 100% nitrogen (group 4).
  
  
  RESULTS
  After 1 h of reperfusion, significant differences were noted between group 1 and groups 2, 3, and 4 in peak airway pressure (27 +/- 5 cm H2O vs. 15 +/- 1 cm H2O, 17 +/- 2 cm H2O, and 16 +/- 1 cm H2O, respectively; P < 0.05), in weight gain (137 +/- 24 vs. 31 +/- 7, 30 +/- 3, and 30 +/- 2%, respectively; P < 0.05), and in veno-arterial oxygen pressure gradient (9 +/- 5 vs. 95 +/- 13, 96 +/- 7 and 96 +/- 4 mmHg, respectively; P < 0.05). Also, wet-to-dry weight ratio at end of reperfusion was significantly different (10.2 +/- 1.0 vs. 6.0 +/- 0.3. 5.2 +/- 0.3 and 5.4 +/- 0.5, respectively; P < 0.05). No significant differences in any of these parameters were observed between groups 2, 3, and 4.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Center for Experimental Surgery and Anesthesiology, Katholieke Universiteit Leuven, Belgium. Dirk.VanRaemdonck@uz.kuleuven.ac.be
authors.forename: D E
authors.initials: DE
authors.lastname: Van Raemdonck
authors.forename: N C
authors.initials: NC
authors.lastname: Jannis
authors.forename: P R
authors.initials: PR
authors.lastname: De Leyn
authors.forename: W J
authors.initials: WJ
authors.lastname: Flameng
authors.forename: T E
authors.initials: TE
authors.lastname: Lerut
mesh_terms: D000818:Animals; D006085:Graft Survival / Q000502:physiology*; D006439:Hemodynamics; D016040:Lung Transplantation / Q000502:physiology*; D009926:Organ Preservation; D011650:Pulmonary Alveoli / Q000502:physiology*; D011817:Rabbits; D015424:Reperfusion; D014655:Vascular Resistance