Carbon monoxide in sepsis. Review uri icon

Overview

MeSH

  • Anti-Inflammatory Agents
  • Apoptosis
  • Dose-Response Relationship, Drug
  • Forecasting
  • Heme Oxygenase (Decyclizing)
  • Humans
  • Lung Diseases
  • Reactive Oxygen Species
  • Signal Transduction
  • Vascular Diseases

MeSH Major

  • Carbon Monoxide
  • Sepsis

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.

publication date

  • November 2007

has subject area

  • Anti-Inflammatory Agents
  • Apoptosis
  • Carbon Monoxide
  • Dose-Response Relationship, Drug
  • Forecasting
  • Heme Oxygenase (Decyclizing)
  • Humans
  • Lung Diseases
  • Reactive Oxygen Species
  • Sepsis
  • Signal Transduction
  • Vascular Diseases

Research

keywords

  • Journal Article
  • Review

Identity

Language

  • eng

Digital Object Identifier (DOI)

  • 10.1089/ars.2007.1762

PubMed ID

  • 17822362

Additional Document Info

start page

  • 2013

end page

  • 2026

volume

  • 9

number

  • 11