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J Thorac Cardiovasc Surg 1998;115:1335-1339
© 1998 Mosby, Inc.


CARDIAC AND PULMONARY REPLACEMENT

Controlled reperfusion and pentoxifylline modulate reperfusion injury after single lung transplantation

Stephen C. Clark, FRCSa, Catherine Sudarshan, FRASa, Rakesh Khanna, FRCSa, Jonathan Roughan, PhDb, Paul A. Flecknell, MRCVSb, John H. Dark, FRCSa

From the Cardiothoracic Centre, Freeman Hospital,a Newcastle upon Tyne, and The University of Newcastle upon Tyne,b Newcastle upon Tyne, United Kingdom.

Received for publication Oct. 13, 1997. Revisions requested Dec. 8, 1997; revisions received Dec. 29, 1997. Accepted for publication Jan. 2, 1997. Address for reprints: Stephen C. Clark, FRCS, The Cardiothoracic Centre, Freeman Hospital, Newcastle upon Tyne, NE7 7DN, United Kingdom.

Abstract

Objective: Rodent models have suggested that initial low-pressure reperfusion of transplanted lungs reduces injury after ischemia. We investigated this phenomenon and the use of pentoxifylline in a porcine model of left single lung transplantation.
Methods: Donor lungs were preserved with Euro-Collins solution for a mean ischemic time of 18.4 hours. Neutrophil trapping in the graft, pulmonary artery pressure, and gas exchange were assessed over a 12-hour period. Partial occlusion of the contralateral pulmonary artery allowed manipulation of the pulmonary artery pressure in the transplanted lung. Group A (n = 5) was perfused at a mean pulmonary artery pressure of 20 mm Hg, group B was reperfused at a mean pulmonary artery pressure of 45 mm Hg for 10 minutes before reducing the pressure to the same as group A, and group C was reperfused at a mean pressure of 20 mm Hg for 10 minutes, then increased to a mean of 45 mm Hg for the remainder of the experiment. Group D was reperfused as in group A with the addition of intravenous pentoxifylline.
Results: Leukocyte sequestration was observed in the first 10 minutes after reperfusion in groups A, B, and C, with maximal sequestration at 2 minutes. Significantly more sequestration was observed in the first 6 minutes in group B than in groups A and C, which were similar. Pentoxifylline significantly reduced leukocyte sequestration. Pulmonary venous oxygen tension in the allograft lung was worst in group B. Groups A and C were similar, but group D was superior to all other groups (p < 0.001).
Conclusions: Low-pressure reperfusion, even when limited to the first 10 minutes, modulates reperfusion injury possibly through a leukocyte-dependent mechanism. The addition of pentoxifylline in the recipient confers significant additional benefit.




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