Carbon monoxide: present and future indications for a medical gas. Review uri icon

Overview

MeSH

  • Administration, Inhalation
  • Animals
  • Dose-Response Relationship, Drug
  • Environmental Pollutants
  • Gases
  • Heme
  • Heme Oxygenase (Decyclizing)
  • Humans
  • Inhalation Exposure
  • Risk Assessment
  • Signal Transduction

MeSH Major

  • Anti-Inflammatory Agents
  • Carbon Monoxide

abstract

  • Gaseous molecules continue to hold new promise in molecular medicine as experimental and clinical therapeutics. The low molecular weight gas carbon monoxide (CO), and similar gaseous molecules (e.g., H2S, nitric oxide) have been implicated as potential inhalation therapies in inflammatory diseases. At high concentration, CO represents a toxic inhalation hazard, and is a common component of air pollution. CO is also produced endogenously as a product of heme degradation catalyzed by heme oxygenase enzymes. CO binds avidly to hemoglobin, causing hypoxemia and decreased oxygen delivery to tissues at high concentrations. At physiological concentrations, CO may have endogenous roles as a signal transduction molecule in the regulation of neural and vascular function and cellular homeostasis. CO has been demonstrated to act as an effective anti-inflammatory agent in preclinical animal models of inflammation, acute lung injury, sepsis, ischemia/reperfusion injury, and organ transplantation. Additional experimental indications for this gas include pulmonary fibrosis, pulmonary hypertension, metabolic diseases, and preeclampsia. The development of chemical CO releasing compounds constitutes a novel pharmaceutical approach to CO delivery with demonstrated effectiveness in sepsis models. Current and pending clinical evaluation will determine the usefulness of this gas as a therapeutic in human disease.

publication date

  • March 2013

has subject area

  • Administration, Inhalation
  • Animals
  • Anti-Inflammatory Agents
  • Carbon Monoxide
  • Dose-Response Relationship, Drug
  • Environmental Pollutants
  • Gases
  • Heme
  • Heme Oxygenase (Decyclizing)
  • Humans
  • Inhalation Exposure
  • Risk Assessment
  • Signal Transduction

Research

keywords

  • Journal Article
  • Review

Identity

Language

  • eng

PubMed Central ID

  • PMC3604600

Digital Object Identifier (DOI)

  • 10.3904/kjim.2013.28.2.123

PubMed ID

  • 23525151

Additional Document Info

start page

  • 123

end page

  • 140

volume

  • 28

number

  • 2