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Ann Thorac Surg 1995;60:962-963
© 1995 The Society of Thoracic Surgeons
University Hospital and the Robarts Research Institute PO Box 5339 London, Ontario N6A 5A5 Canada
The practice of lung transplantation has been constrained by a marked shortage of donor organs. Studies have revealed that only a small percentage of potential donors have lungs that are suitable for transplantation because of aspiration pneumonitis, infection, neurogenic pulmonary edema, iatrogenic overhydration, lung contusion, and less commonly preexisting pulmonary disease in the donor [1–3]. Even in cases of ``optimal'' donor lungs, graft preservation times are limited to 6 to 8 hours and pulmonary dysfunction after transplantation is not uncommon [4, 5]. New strategies to improve the preservation of lung grafts are thus essential. Whereas promising work in this area has been undertaken recently in the experimental laboratory, these studies have usually focused on the long-term preservation of normal lungs for transplantation [4]. This article by Dr Sasaki and colleagues from the New England Deaconess Hospital is therefore topical and important because it addresses the preservation of compromised lungs in a previously validated model of endotoxin-mediated rat lung injury [6].
There are a number of shortcomings to this article that will need to be addressed in future studies. First, there is a danger in extrapolating lipopolysaccharide-induced lung injury in rats to established pulmonary damage in human lung donors. The New England Deaconess group and other groups may wish to establish other experimental models of injured donor lungs (eg, aspiration, mild to moderate lung edema, ventilation-induced injury) that may be more relevant to the clinical situation of compromised donor lung grafts. Second, this article would have been strengthened by including additional experimental groups of normal (ie, nonseptic) rat lungs that have been stored for 6 and 12 hours, rather than comparing the preservation of lipopolysaccharide-injured rat lungs with that of historical controls. Third, it is evident that the group 1 animals were not strictly suitable controls, in that they did not undergo 24 hours of internal jugular venous catheterization before operation. Ideally, these control animals should have had an internal jugular venous catheter placed and should have received normal saline solution over 24 hours to mimic the interventions carried out in groups 2, 3 and 4. Fourth, Sasaki and associates chose to flush the lungs in all four experimental groups with physiologic saline solution but added an additional flush with University of Wisconsin solution in group 3 and 4 animals. Ideally, the lungs in all experimental groups should have been flushed in an identical manner to minimize the possible impact of confounding variables.
Finally, the ready extrapolation of results in this isolated, perfused model of compromised rat lungs to the clinical situation appears premature. Sasaki and associates' concluding statement should be tempered by the realization that further studies in an in vivo, large-animal lung transplant model in which compromised donor lungs have been used is an important next step. Overall, however, this article is of value because of its innovative and rigorous approach in assessing ischemia-reperfusion injury in compromised donor lungs. Further work in this area, using other more clinically relevant models of donor lung injury, is required to expand the pool of donor lungs and alleviate the severe organ shortage that currently limits clinical lung transplantation.
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