title: Effects of hypercapnia on the lung.
abstract: Gases are sensed by lung cells and can activate specific intracellular signalling pathways, and thus have physiological and pathophysiological effects. Carbon dioxide (CO2), a primary product of oxidative metabolism, can be sensed by eukaryotic cells eliciting specific responses via recently identified signalling pathways. However, the physiological and pathophysiological effects of high CO2(hypercapnia) on the lungs and specific lung cells, which are the primary site of CO2elimination, are incompletely understood. In this review, we provide a physiological and mechanistic perspective on the effects of hypercapnia on the lungs and discuss the recent understanding of CO2modulation of the alveolar epithelial function (lung oedema clearance), epithelial cell repair, innate immunity and airway function.
authors.affiliation: Division of Pulmonary and Critical Care Medicine, Northwestern University, Chicago, IL, USA.
authors.forename: Masahiko
authors.initials: M
authors.lastname: Shigemura
authors.affiliation: Division of Pulmonary and Critical Care Medicine, Northwestern University, Chicago, IL, USA.
authors.forename: Emilia
authors.initials: E
authors.lastname: Lecuona
authors.affiliation: Division of Pulmonary and Critical Care Medicine, Northwestern University, Chicago, IL, USA.
authors.forename: Jacob I
authors.identifier: 0000-0002-2089-4764
authors.initials: JI
authors.lastname: Sznajder
mesh_terms: D000818:Animals; D002245:Carbon Dioxide / Q000378:metabolism; D006801:Humans; D006935:Hypercapnia / Q000378:metabolism* / Q000473:pathology; D007113:Immunity, Innate / Q000502:physiology*; D008168:Lung / Q000378:metabolism* / Q000473:pathology; D011650:Pulmonary Alveoli / Q000378:metabolism / Q000473:pathology
chemical_list: D002245:Carbon Dioxide
keywords: airway function; alveolar epithelial function; carbon dioxide; hypercapnia; injury and repair; innate immunity and host defense