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Ann Thorac Surg 1994;57:715-722
© 1994 The Society of Thoracic Surgeons
Division of Cardiothoracic Surgery and Departments of Anesthesiology, Radiology, and Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania USA
Accepted for publication June 28, 1993.
* Address reprint requests to Dr Aeba, Division of Cardiac Surgery, Department of Surgery, Keio University, 35 Shinanomachi, Shinjuku, Tokyo 160, Japan.
The records of 100 lung transplant recipients (13 heart-lungs, 45 double-lungs, and 42 single-lungs) from September 1990 through April 1992 were reviewed to determine the role of cardiopulmonary bypass (CPB) in early graft dysfunction. Fifty-five patients requiring CPB (CPB group) for 186 ± 54 minutes were compared with the 45 patients without CPB (no-CPB group). All of the heartlung and en-bloc double-lung transplantations were petformed under CPB, with pulmonary vascular lung disease the principal diagnosis, resulting in a significantly younger age population in the CPB group. All other donor- and recipient-related factors matched well in both groups. Of 38 bilateral single-lung transplantations, CPB was used in 18. In double-lung and heart-lung recipients gas exchange of the allografts was evaluated by the arterial/alveolar oxygen tension ratios at nine intervals during the first 72 hours. The mean arterial/alveolar oxygen tension ratio in the CPB group was 0.48 ± 0.19, significantly lower than in the no-CPB group with 0.60 ± 0.22 (p = 0.025). All patients had radiographic interpretation and scoring of pulmonary infiltrates from chest roentgenograms taken within 12 hours after reperfusion. The CPB group had more severe pulmonary infiltrates than the no-CPB group (p = 0.034). Prolonged intubation defined as 7 days or longer occurred significantly more often ( [equation]) in the CPB group than in the no-CPB group ( [equation]) (p = 0.003). Actuarial graft and patient survival at 1 month was better in the no-CPB group than in the CPB group ( [equation] versus [equation] [p = 0.05] and [equation] versus [equation] [p = 0.033], respectively). These results suggest that the interaction between CPB and preservation injury exaggerates pulmonary dysfunction in clinical lung transplantation.
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