Carbon monoxide in exhaled breath testing and therapeutics.

Abstract

Carbon monoxide (CO), a low molecular weight gas, is a ubiquitous environmental product of organic combustion, which is also produced endogenously in the body, as the byproduct of heme metabolism. CO binds to hemoglobin, resulting in decreased oxygen delivery to bodily tissues at toxicological concentrations. At physiological concentrations, CO may have endogenous roles as a potential signaling mediator in vascular function and cellular homeostasis. Exhaled CO (eCO), similar to exhaled nitric oxide (eNO), has been evaluated as a candidate breath biomarker of pathophysiological states, including smoking status, and inflammatory diseases of the lung and other organs. eCO values have been evaluated as potential indicators of inflammation in asthma, stable COPD and exacerbations, cystic fibrosis, lung cancer, or during surgery or critical care. The utility of eCO as a marker of inflammation and its potential diagnostic value remain incompletely characterized. Among other candidate 'medicinal gases' with therapeutic potential, (e.g., NO and H2S), CO has been shown to act as an effective anti-inflammatory agent in preclinical animal models of inflammatory disease, acute lung injury, sepsis, ischemia/reperfusion injury and organ graft rejection. Current and future clinical trials will evaluate the clinical applicability of this gas as a biomarker and/or therapeutic in human disease.

• Authors: Stefan W Ryter, Augustine M K Choi
• Journal: Journal of breath research (J Breath Res) Vol. 7 Issue 1 Pg. 017111 (Mar 2013) ISSN: 1752-7163 [Electronic] England
• PMID: 23446063 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Biomarkers
• Carbon Monoxide
• HMOX1 protein, human
• Heme Oxygenase-1

Topics

• Acute Lung Injury (prevention & control)
• Anesthesia
• Animals
• Asthma (metabolism)
• Biomarkers (metabolism)
• Breath Tests
• Carbon Monoxide (metabolism, pharmacology, therapeutic use)
• Cystic Fibrosis (metabolism)
• Environmental Exposure
• Exhalation
• Graft Rejection (prevention & control)
• Heme Oxygenase-1 (physiology)
• Humans
• Inflammation (drug therapy)
• Organ Transplantation
• Postoperative Period
• Pulmonary Disease, Chronic Obstructive (metabolism)
• Reperfusion Injury (prevention & control)
• Respiration, Artificial
• Respiratory Tract Infections (metabolism)
• Sepsis (drug therapy)
• Smoking (metabolism)
• Ventilator-Induced Lung Injury (prevention & control)