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Ann Thorac Surg 2001;72:1171-1172
© 2001 The Society of Thoracic Surgeons

Invited commentary

John A. Kern, MDa

a TCV Surgery, University of Virginia, Lee St, Charlottesville, VA 22908, USA

e-mail: jak3r@virginia.edu

Despite significant advances in organ procurement and preservation techniques, transplanted lungs are unusually sensitive to ischemia-reperfusion injury. Severe early graft dysfunction has been reported in up to 20% of lung recipients, and this early dysfunction can lead to an increase in early and late morbidity and mortality. Although ischemia plays an important role in initiating early post-transplant lung injury, reperfusion mechanisms are equally important. Pulmonary ischemia-reperfusion (I/R) injury is a complex process involving many cell types and inflammatory biochemical mediators. The study by Sunose and colleagues has utilized a popular dog model of lung transplantation to evaluate the effect of a COX-2 inhibitor on subsequent graft function after 12 hours of ischemia and varying times of up to 4 hours of reperfusion. The hilum of the contralateral non-transplanted lung was ligated in order to evaluate the function of the transplanted organ and its ability to support the animal. The . . . [Full Text of this Article]


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Effect of a cyclooxygenase-2 inhibitor, FK3311, in a canine lung transplantation model
Yutaka Sunose, Izumi Takeyoshi, Hirofumi Tsutsumi, Susumu Ohwada, Noboru Oriuchi, Koshi Matsumoto, and Yasuo Morishita
Ann. Thorac. Surg. 2001 72: 1165-1171. [Abstract] [Full Text] [PDF]






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