Effect of inflation on adenosine triphosphate catabolism and lactate production during normothermic lung ischemia

Abstract

Although few biochemical data comparing adenosine triphosphate (ATP) catabolism or lactate production in isolated deflated versus inflated lung tissue are available, most transplant centers preserve their donor lungs inflated. We measured ATP level (using high-performance liquid chromatography), energy charge, and lactate level during 2 hours of normothermic ischemia in deflated lung tissue (n = 6), in lung tissue inflated with room air (n = 6), and in lung tissue inflated with 100% oxygen (n = 6). To determine the onset of anaerobic metabolism in lung issue inflated with 100% O 2, ATP and lactate levels were measured in another group (n = 6) during 8 hours of normothermic ischemia. Rabbit lungs were flushed in situ with a modified Krebs-Henseleit solution (60 mL/kg). They were isolated and immersed in 0.9% Nacl at 37 °C. In deflated lung tissue, ATP level (control value, 9.4 ± 0.58 μmol/g dry wt) decreased and lactate level (control value, 5.6 ± 1.16 μmol/g dry wt) increased after 15 minutes of ischemia (ATP, 5.2 ± 0.86 μmol/g dry wt; lactate, 13.3 ± 1.58 μmol/g dry wt). When the lung was stored inflated with room air, ATP breakdown and increase of lactate concentration only occurred after 90 minutes of normothermic ischemia (at 60 minutes: ATP, 8.0 ± 0.58 μmol/g dry wt; lactate, 6.3 ± 1.1 μmol/g dry wt). In lungs stored inflated with 100% O 2, ATP breakdown and lactate accumulation only occurred after 5 hours of normothermic ischemia (at 4 hours: ATP, 8.1 ± 0.74 μmol/g dry wt; lactate, 5.9 ± 1.28 μmol/g dry wt). These data suggest that the breakdown of ATP and the onset of anaerobic metabolism in lung tissue is related to the alveolar oxygen concentration during storage, and that in the isolated inflated lung, aerobic metabolism continues for 4 hours even when perfusion has stopped.