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Ann Thorac Surg 2000;70:264-269
© 2000 The Society of Thoracic Surgeons
a Division of Thoracic and Cardiovascular Surgery, Department of Surgery, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas, USA
c Division of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas, USA
b Department of Radiology, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas, USA
d Dallas Veterans Affairs Medical Center, Dallas, Texas, USA
Address reprint requests to Dr Dan Meyer, Division of Thoracic and Cardiovascular Surgery, Department of Surgery, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75235
e-mail: dan.meyer{at}email.swmed.edu
Presented in part at the Forty-sixth Annual Meeting of the Southern Thoracic Surgical Association, San Juan, Puerto Rico, Nov 46, 1999.
Background. Lung transplantation requires a period of storage and ischemia; we examined the largely unknown effects of that period on intermediary metabolism.
Methods. Two groups of isolated rat lung blocks (n = 16 each) were flushed with Euro-Collins solution and harvested. The lung blocks were immediately ventilated and either perfused for 30 minutes with an erythrocyte-based solution containing carbon 13 labeled substrates (group 1) or stored for 6 hours at 1°C and then reperfused (group 2). Half of each group was reperfused at a physiologic PO2 the other half at high PO2. Analysis of carbon 13 isotopomers was performed to determine substrate utilization through aerobic pathways in lung tissue.
Results. Lungs from both groups oxidized all major substrates. The contribution of fatty acids to acetyl-coenzyme acid oxidized in the citric acid cycle was significantly higher in group 2 than in group 1 (31.3% ± 2.2% versus 22.0% ± 2.1%, p < 0.05). Perfusate PO2 did not affect substrate preference. Gas exchange was worse in stored lungs.
Conclusions. After a period of hypothermic ischemia and storage, substrate preference in lung tissue exhibits a switch towards fatty acids. As fatty acid oxidation occurring after ischemia is deleterious in other organs, strategies to inhibit this process in stored lungs may warrant further investigation.
Related Article
Ann. Thorac. Surg. 2000 70: 269.
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