Journal article
Authors list: Vadasz, Istvan; Hubmayr, Rolf D.; Nin, Nicolas; Sporn, Peter H. S.; Sznajder, Jacob I.
Publication year: 2012
Pages: 417-421
Journal: American Journal of Respiratory Cell and Molecular Biology
Volume number: 46
Issue number: 4
ISSN: 1044-1549
eISSN: 1535-4989
Open access status: Green
DOI Link: https://doi.org/10.1165/rcmb.2011-0395PS
Publisher: American Thoracic Society
Abstract:
Patients with severe acute and chronic lung diseases develop derangements in gas exchange that may result in increased levels of CO2 (hypercapnia), the effects of which on human health are incompletely understood. It has been proposed that hypercapnia may have beneficial effects in patients with acute lung injury, and the concepts of "permissive" and even "therapeutic" hypercapnia have emerged. However, recent work suggests that CO2 can act as a signaling molecule via pH-independent mechanisms, resulting in deleterious effects in the lung. Here we review recent research on how elevated CO2 is sensed by cells in the lung and the potential harmful effects of hypercapnia on epithelial and endothelial barrier, lung edema clearance, innate immunity, and host defense. In view of these findings, we raise concerns about the potentially deleterious effects hypercapnia may have in patients with acute and chronic lung diseases.
Citation Styles
Harvard Citation style: Vadasz, I., Hubmayr, R., Nin, N., Sporn, P. and Sznajder, J. (2012) Hypercapnia: A Nonpermissive Environment for the Lung, American Journal of Respiratory Cell and Molecular Biology, 46(4), pp. 417-421. https://doi.org/10.1165/rcmb.2011-0395PS
APA Citation style: Vadasz, I., Hubmayr, R., Nin, N., Sporn, P., & Sznajder, J. (2012). Hypercapnia: A Nonpermissive Environment for the Lung. American Journal of Respiratory Cell and Molecular Biology. 46(4), 417-421. https://doi.org/10.1165/rcmb.2011-0395PS
Keywords
alveolar epithelial barrier function; ALVEOLAR EPITHELIAL-CELLS; HOST-DEFENSE; Na,K-ATPase; TIDAL VOLUMES; VENTILATION STRATEGY