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10.1113/JP273781

http://scihub22266oqcxt.onion/10.1113/JP273781
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suck abstract from ncbi


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pmid28044311
      J+Physiol 2017 ; 595 (8 ): 2431-2437
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  • Effects of hypercapnia on the lung #MMPMID28044311
  • Shigemura M ; Lecuona E ; Sznajder JI
  • J Physiol 2017[Apr]; 595 (8 ): 2431-2437 PMID28044311 show ga
  • Gases are sensed by lung cells and can activate specific intracellular signalling pathways, and thus have physiological and pathophysiological effects. Carbon dioxide (CO(2) ), 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 CO(2) (hypercapnia) on the lungs and specific lung cells, which are the primary site of CO(2) elimination, 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 CO(2) modulation of the alveolar epithelial function (lung oedema clearance), epithelial cell repair, innate immunity and airway function.
  • |Animals [MESH]
  • |Carbon Dioxide/metabolism [MESH]
  • |Humans [MESH]
  • |Hypercapnia/*metabolism/pathology [MESH]
  • |Immunity, Innate/*physiology [MESH]
  • |Lung/*metabolism/pathology [MESH]


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