Reactive species and pulmonary edema

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.

Keywords::

• antioxidants
• free radicals
• pulmonary edema
• reactive oxygen and nitrogen species
• RONS
• sodium transport

Acknowledgements

This article is dedicated to the memory of Charles A Bosworth, PhD.

Financial & competing interests disclosure

This work was supported by grants U01 ES015676 and U54 ES017218 from the NIH to Sadis Matalon. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

The authors thank Teri Potter for her superb editorial assistance. No other writing assistance was utilized in the production of this manuscript.