ArticleIntensive care medicine experimental2026
Selective hemoadsorption of cytokines and platelet-neutrophil complexes mitigates lung microvascular hyperpermeability in an ovine acute lung injury model.
Article in Intensive care medicine experimental, 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
backgroundAcute respiratory distress syndrome (ARDS) is a life-threatening disease that is characterized by noncardiogenic pulmonary edema, respiratory distress, and hypoxemia, and has high mortality. Uncontrolled activation of neutrophils and formation of platelet-neutrophil complexes (PNCs) contribute significantly to its pathogenesis. In this study, we investigated whether suppression of systemic inflammation through simultaneous adsorption of inflammatory mediators, including PNCs, reduces lung invasion and offers an effective treatment strategy for ARDS. MATERIALS AND
methodsWe investigated the efficacy of a novel hemoadsorption column, NOA-001, which simultaneously removes cytokines and PNCs, in an ovine model of smoke inhalation-induced ARDS. Animals were assigned to two groups: treatment with NOA-001 (n = 6) or a control group with a blood circuit without the column (n = 5). The impact on neutrophil dynamics, lung injury, edema formation, and inflammatory markers was assessed.
resultsNeutrophil capture rates by NOA-001 were significantly higher at 4 and 6 h compared to controls, with a trend toward lower circulating neutrophil counts. Flow cytometry confirmed that NOA-001 predominantly removed PNCs (CD62
conclusionsSimultaneous removal of cytokines and PNCs using NOA-001 significantly reduced ARDS severity by attenuating pulmonary edema and improving pulmonary gas exchange. These results suggest that NOA-001 may be a novel and promising therapeutic strategy for ARDS.
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