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Endothelial Activation in ARDS*

Guy A. Zimmerman, MD; Kurt H. Albertine, PhD; Holly J. Carveth, MD; Edward A. Gill, MD; Colin K. Grissom, MD; John R. Hoidal, MD; Tada-atsu Imaizumi, MD; Christopher G. Maloney, MD; Thomas M. McIntyre, PhD; John R. Michael, MD; James F. Orme, MD; Stephen M. Prescott, MD; Matthew S. Topham, MD
Author and Funding Information

*From the University of Utah Special Center of Research in ARDS, University of Utah Health Sciences Center, Salt Lake City, UT.

Correspondence to: Guy A. Zimmerman, MD, University of Utah, CVRTI, 95 S 2000 E, Salt Lake City, UT 84112-5000; e-mail: guy_zimmerman@gatormail.cvrti.utah.edu



Chest. 1999;116(suppl_1):18S-24S. doi:10.1378/chest.116.suppl_1.18S
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Extract

Endothelial injury is often identified as a hallmark of ARDS.16 Yet endothelial cells may be altered in other ways besides frank injury in ARDS and in other pathologic syndromes. A major concept in vascular biology that has largely evolved since the time of the original description of ARDS is that endothelial cells can become activated and that this can occur independently of, or as a component or consequence of, cellular injury.8 Endothelial activation is now considered by some clinicians and investigators to be a principal mechanism in the complex pathologic events that result in ARDS.10 This broadened concept of a spectrum of endothelial alterations—including cellular activation—in response to factors such as sepsis, trauma, oxidant and chemical attack, and other insults has merit, but several questions also merit consideration.


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