Abstract
Oxygen-derived free radicals (ROS) have been identified to contribute significantly to ischemia–reperfusion (I/R) injury by initiating chain reactions with polyunsaturated membrane lipids (lipid peroxidation, LPO) resulting in the generation of several aldehydes and ketones. Due to their volatile nature these LPO products can be measured noninvasively in breath. We hypothesized that one of these markers, namely propionaldehyde, will be increased in lung and heart–lung transplant patients where severe oxidative stress due to I/R injury with early graft dysfunction represents one of the major postoperative complications resulting in prolonged ventilation and increased in-hospital morbidity and mortality. Expiratory air measurements for acetone, isoprene, and propionaldehyde were performed in seven patients after lung (n=5) or heart–lung (n=2) transplantation, ventilated patients (n=12), and healthy volunteers (n=17) using online ion-molecule reaction mass spectrometry. Increased concentrations of acetone (transplanted: 3812 [2347–12498]; ventilated: 1255 [276–1959]; healthy: 631 [520–784] ppbv; P<.001) and propionaldehyde (transplanted: 270 [70–424]; ventilated: 82 [41.8–142]; healthy: 1.7 [0.1–11.8] ppbv; P<.001) were found in expiratory air of transplanted and ventilated patients. Propionaldehyde resulting from spontaneous fragmentation of peroxides due to free radical-induced LPO after I/R injury in patients after lung or heart–lung transplantation can be quantified in expired breath.
Published Version
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