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Hypocapnia, mitochondria and surfactant secretion
  1. Beata Kosmider1,2,3,
  2. Karim Bahmed1,2,
  3. Steven Kelsen1,2
  1. 1 Department of Thoracic Medicine and Surgery, Temple University, Philadelphia, Pennsylvania, USA
  2. 2 Center for Inflammation, Translational and Clinical Lung Research, Temple University, Philadelphia, Pennsylvania, USA
  3. 3 Department of Physiology, Temple University, Philadelphia, Pennsylvania, USA
  1. Correspondence to Dr Beata Kosmider; beata.kosmider{at}temple.edu

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Surfactant, a phospholipoprotein produced and stored by alveolar type II (ATII) cells, lowers surface tension in the alveolus and distal airways and is essential for normal lung mechanics and gas exchange.1 Decreases in surfactant production induced by prematurity or disease cause alveolar collapse, hypoxemia and reductions in lung compliance, thereby requiring greater distending pressures to inflate the lung and increases in the work of breathing.2 Prior studies dating back >30 years have shown that alveolar hypocapnia causes depletion of lamellar bodies in ATII cells and decreases surfactant production.3 However, the mechanism(s) underlying the effect(s) of hypocapnia on surfactant secretion by ATII cells are not well understood.

The paper by Kiefmann et al 4 in Thorax sheds light on molecular mechanisms which may contribute to the effects of alveolar hypocapnia on surfactant production in vivo. The authors examined surfactant secretion, cytosolic and mitochondrial calcium and alveolar volume and compliance in two rodent preparations: isolated, blood-perfused rat lungs …

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