ArticleJournal of translational medicine2026
Severe hyperoxia during VA-ECMO promotes oxidative stress and multi-organ injury in an experimental rat model of septic cardiomyopathy.
Article in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundSevere hyperoxia during venoarterial extracorporeal membrane oxygenation (VA-ECMO) has been associated with adverse clinical outcomes in observational studies. However, causal evidence and optimal oxygen targets remain uncertain. Hyperoxia may exacerbate oxidative stress and organ injury, particularly in the presence of systemic inflammation and ischemic shock. This study aimed to investigate the dose-dependent effects of membrane lung sweep oxygen fraction (FsO₂) during the early phase of VA-ECMO on systemic oxidative stress and early multi-organ injury markers, and to explore the mechanistic role of reactive oxygen species (ROS) using a rat VA-ECMO model.
methodsIn this randomized experimental study, Sprague-Dawley rats were divided into normal rats and rats with cardiogenic shock induced by septic cardiomyopathy using LPS. Graded membrane FsO
resultsGraded FsO₂ levels produced distinct and stable differences in arterial PaO₂ and SaO₂ during VA-ECMO support. In both normal and shock rats, severe hyperoxia (FsO₂ = 90%) caused greater systemic oxidative stress, metabolic acidosis and structural injury in the lung, liver, and kidney than normoxia (FsO₂ = 30%) or moderate hyperoxia (FsO₂ = 60%). In contrast, myocardial injury was not significantly modified by FsO₂ gradients. In animals without shock, these hyperoxia-associated changes were relatively mild and largely attenuated after VA-ECMO withdrawal, whereas shock markedly increased susceptibility to severe hyperoxia-induced early multi-organ injury. Notably, moderate hyperoxia (FsO₂ = 60%) was not associated with clearly worse oxidative stress or organ damage than normoxia (FsO₂ = 30%) in either normal or shock animals. Tempol administration attenuated oxidative stress and mitigated histological injury, and diminished differences among FsO₂ groups.
conclusionsIn this early-phase rat model of septic cardiomyopathy requiring VA-ECMO support, severe hyperoxia (FsO CLINICAL TRIAL NUMBER: Not applicable.
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