Viña, José, Emilio Servera, Miguel Asensi, Juan Sastre, Federico V. Pallardó, José A. Ferrero, JoséGarcı́a-de-la-Asunción, Vicente Antón, and Julio Marı́n. Exercise causes blood glutathione oxidation in chronic obstructive pulmonary disease: prevention by O2therapy. J. Appl. Physiol. 81(5): 2199–2202, 1996.—The aim of the present study was to determine whether glutathione oxidation occurs in chronic obstructive pulmonary disease (COPD) patients who perform exercise and whether this could be prevented. Blood glutathione red-ox ratio [oxidized-to-reduced glutathione (GSSG/GSH)] was significantly increased when patients performed exercise for a short period of time until exhaustion. Their resting blood GSSG/GSH was 0.039 ± 0.008 (SD) ( n = 5), whereas after exercise it increased to 0.085 ± 0.019, P < 0.01. Glutathione oxidation associated with exercise was partially prevented by oxygen therapy (resting value: 0.037 ± 0.014, n = 5; after exercise: 0.047 ± 0.016, n = 5, P < 0.01). We conclude that light exercise causes an oxidation of glutathione in COPD patients, which can be partially prevented by oxygen therapy.
Limb RIPC decreased EBC 8-isoprostane levels and other oxidative lung injury markers during lung lobectomy. RIPC also improved postoperative gas exchange as measured by PaO2/FiO2 ratio.
During lung lobectomy, the operated lung is collapsed and oxidative injury occurs, with the levels of markers of oxidative stress increasing simultaneously in exhaled breath condensate and blood during one-lung ventilation. These increases were larger after resuming two-lung ventilation. Increases immediately before resuming two-lung ventilation and immediately after resuming two-lung ventilation were directly correlated with the duration of one-lung ventilation.
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