Abstract
Carbon monoxide (CO), like nitric oxide (NO), has been reported to have biologic actions such as smooth muscle relaxation1 or inhibition of platelet aggregation,2 and to act as a neural messenger in the brain.3,4 CO is produced endogenously in many tissues of the body by the class of enzymes known collectively as heme oxygenase (HO).5 Two forms of HO have been characterized. Of these, HO-1 is present in the pulmonary vascular endothelium,6 alveolar macrophages7 and human airway epithelium,8 and is induced by oxidative stress,6,9 inflammatory cytokines,10,11 and NO.12 HO-2 is not inducible and is widely distributed throughout the body, with high concentrations in the brain.5 CO can be detected in exhaled air in smokers and non-smokers.13 The pathogenesis of inflammatory respiratory diseases is associated with several factors including oxidative stress and inflammatory cytokines. Therefore, we studied whether the levels of exhaled CO increase in patients with inflammatory respiratory diseases.
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Yamaya, M., Okinaga, S., Sekizawa, K., Monma, M., Sasaki, H. (2002). Increased Carbon Monoxide in Exhaled Air in Patients with Inflammatory Respiratory Diseases. In: Abraham, N.G. (eds) Heme Oxygenase in Biology and Medicine. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0741-3_7
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DOI: https://doi.org/10.1007/978-1-4615-0741-3_7
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