Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2007 Nov;9(11):2013-26.
doi: 10.1089/ars.2007.1762.

Carbon monoxide in sepsis

Affiliations
Review

Carbon monoxide in sepsis

Alexander Hoetzel et al. Antioxid Redox Signal. 2007 Nov.

Abstract

Despite modern practices in critical care medicine, sepsis or systemic inflammatory response syndrome remains a leading cause of morbidity and mortality in the intensive care unit. Thus, the need to identify new therapeutic tools for the treatment of sepsis is urgent. In this context, carbon monoxide has become a promising therapeutic molecule that can potentially prevent uncontrolled inflammation in sepsis. In humans, carbon monoxide arises endogenously from the degradation of heme by heme oxygenase enzymes. Both endogenously synthesized and exogenously applied carbon monoxide can exert antiinflammatory and antiapoptotic effects in cells and tissues. Based on these properties, carbon monoxide, when applied at low concentration, conferred protection in a variety of cellular and rodent models of sepsis, and furthermore reduced morbidity and mortality in vivo. Therefore, application of carbon monoxide may have a major impact on the future of sepsis treatment. This review summarizes evidence for salutary effects of carbon monoxide in sepsis of various organs, including lung, heart, kidney, liver, and intestine, and discusses the potential translation of the data into human clinical trials.

PubMed Disclaimer

Publication types

MeSH terms

LinkOut - more resources