Propofol attenuates lung endothelial injury induced by ischemia-reperfusion and oxidative stress

Irina V. Balyasnikova, David J. Visintine, Helena B. Gunnerson, Chanannait Paisansathan, Verna L. Baughman, Richard D. Minshall, Sergei M. Danilov*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

55 Scopus citations


Lung dysfunction after cardiopulmonary bypass and lung transplantation results from oxidant-mediated cellular damage. Previously, we observed the shedding of angiotensin-converting enzyme (ACE) from the endothelial cell surface to be a more sensitive and earlier marker of oxidative lung endothelial injury than lung wet-to-dry weight ratio. The aim of this study was to evaluate the potential of the anesthetic propofol, which has antioxidant properties, to prevent oxidative lung injury by measuring ACE shedding. ACE release from isolated perfused rat lungs increased significantly after ischemia-reperfusion (I/R). Propofol significantly decreased I/R-induced ACE release by 23.4% (P < 0.05). Perfusion with 0.75 mM H2O2 also caused ACE release from the lung microvasculature, which was similarly attenuated by propofol. The protective effect of propofol on H2O 2-induced ACE shedding was confirmed in vitro using Chinese Hamster Ovary cells overexpressing human ACE. Thus, propofol can attenuate oxidative injury of the pulmonary endothelium as detected by ACE shedding in I/R and H2O2 models of acute lung injury.

Original languageEnglish (US)
Pages (from-to)929-936
Number of pages8
JournalAnesthesia and Analgesia
Issue number4
StatePublished - Apr 1 2005

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine


Dive into the research topics of 'Propofol attenuates lung endothelial injury induced by ischemia-reperfusion and oxidative stress'. Together they form a unique fingerprint.

Cite this