Reactive species and pulmonary edema
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Updated: Jun 14, 2026

Halogenated Agent Delivery in Porcine Model of Acute Respiratory Distress Syndrome via an Intensive Care Unit Type Device
Published on: September 24, 2020
Karen E Iles1, Weifeng Song, David W Miller
1Department of Anesthesiology, University of Alabama at Birmingham, 901 19th Street South, 304 BMR II, Birmingham, AL 35294-2172, USA, Tel.: +1 205 975 2761, , kiles@uab.edu and Department of Environmental Health Sciences, School of Public Health, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Abstract:
Pulmonary edema occurs when fluid flux into the lung interstitium exceeds its removal, resulting in hypoxemia and even death. Noncardiogenic pulmonary edema (NPE) generally results when microvascular and alveolar permeability to plasma proteins increase, one possible etiology being oxidant injury. Reactive oxygen and nitrogen species (RONS) can modify or damage ion channels, such as epithelial sodium channels, which alters fluid balance. Experimental systems in which either RONS are increased or protective antioxidant mechanisms are decreased result in alterations of epithelial sodium channel activity and support the hypothesis that RONS are important in NPE. Both basic and clinical studies are needed to critically define the RONS-NPE connection and the capacity of antioxidant therapy (either alone or as a supplement to β-agonists) to improve patient outcome.
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