Editorial Views  |   July 2018
Should We Stop for Growth Arrest-specific 6 in Acute Respiratory Distress Syndrome?
Author Notes
  • From the Department of Anesthesiology, University of California, San Francisco, San Francisco, California.
  • Corresponding article on page 143.
    Corresponding article on page 143.×
  • Accepted for publication February 27, 2018.
    Accepted for publication February 27, 2018.×
  • Address correspondence to Dr. Lee: jae-woo.lee@ucsf.edu
Article Information
Editorial Views / Critical Care / Respiratory System
Editorial Views   |   July 2018
Should We Stop for Growth Arrest-specific 6 in Acute Respiratory Distress Syndrome?
Anesthesiology 7 2018, Vol.129, 8-10. doi:10.1097/ALN.0000000000002204
Anesthesiology 7 2018, Vol.129, 8-10. doi:10.1097/ALN.0000000000002204
LOW tidal volume mechanical ventilation is the primary supportive therapy for critically ill patients with acute respiratory distress syndrome. Surprisingly, despite widespread acknowledgment of its protective effects and implementation, overall mortality rates in acute respiratory distress syndrome have remained relatively unchanged.1  Due to the patchy nature of the injury, a possible explanation may be a deleterious effect of even low tidal volume mechanical ventilation in acute respiratory distress syndrome, overdistention of “normal” aerated lung resulting in inflammation and dysfunction. During mechanical ventilation, the flow of gas into the lung takes the path of least resistance. Areas of the lung that are collapsed (atelectasis) or consolidated or filled with secretions as in acute respiratory distress syndrome will be underinflated, while those areas that are relatively normal will be overinflated, becoming overdistended and injured. Consequently, more research is needed to better understand the inflammatory injury within the “baby” lung during acute respiratory distress syndrome. Recently, growth arrest-specific 6 (Gas6), an endogenous agonist of an antiinflammatory receptor with known immunomodulatory properties, Axl, was found to be elevated in patients with sepsis, the leading cause of acute respiratory distress syndrome.2  In this month’s issue of Anesthesiology, Otulakowski et al. sought to determine whether high tidal volume mechanical ventilation in mice, a preclinical model of overdistension in acute respiratory distress syndrome, resulted in changes to known antiinflammatory receptor pathways such as Axl.3 
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