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Reactive oxygen species have been implicated in the pathophysiology of lung injury associated with the sequence of ischemia-reperfusion. To study this, we measured the exhaled breath hydrogen peroxide concentration [H2O2] in human and canine models of reperfusion lung injury. Our models were patients subjected to cardiopulmonary bypass (CPB) (Group 1), patients undergoing pulmonary thromboendarterectomy (Group 2), canine single lung transplant (Group 3), and patients subjected to peripheral ischemia resulting from aortic cross-clamping or tourniquet application (Group 4). In addition, we studied two groups with severe lung injury as positive controls. These consisted of hydrochloric acid (HC1)-induced canine lung injury (Group 5) and patients with adult respiratory distress syndrome (Group 6). The exhaled H2O2 was collected by using a −2°C glass coil and assayed by a spectrophotometric method. In Group 1 samples were collected before and immediately after CPB. Group 2 samples were obtained before CPB, immediately after CPB, 3 h later, and daily until extubation. Samples in Group 3 were collected before lung transplant, and hourly for 3 h beginning immediately afterward. Group 4 samples were collected at the onset of reperfusion. Samples from Group 5 were collected before HC1 and after HC1 injury, at 0.5–1.5 and 2–3 h. Group 6 samples were collected when criteria for adult respiratory distress syndrome were met. Groups 1, 3, and 4 exhibited no significant increases in exhaled [H2O2] compared to control values. Group 2 had significantly increased [H2O2] (5.59 ± 3.07 × 10−7 mol/L, P = 0.028) on postoperative Day 2, but there was no correlation of [H2O2] with physiologic indicators of lung injury. Group 5 had a dramatic increase in the [H2O2] in the first post-HC1 sample period (14.92 × 10−7 mol/L ± 9.74 × 10−7 mol/L, P = 0.046), which correlated inversely with the respiratory index. Group 6 had significant increases in [H2O2] (5.45 ± 2.02 × 10−7 mol/L). In conclusion, exhaled H2O2 was not increased immediately after reperfusion in any of the ischemia-reperfusion models but was significantly increased by postoperative Day 2 in the pulmonary thromboendarterectomy patients and in the control groups with severe lung injury. These findings suggest that H2O2 may be a mediator of, or marker for, diverse types of lung injury. However, the temporal sequence of pathophysiologic events and the exact significance of increased exhaled H2O2 is unclear at this time.