Abstract
Nitric oxide (NO) plays a central role in the physiology and pathophysiology of many human organ systems. In the context of the respiratory system, NO promotes vascular and bronchial dilation and is a key mediator of the coordinated beating of ciliated epithelial cells. It also promotes mucus secretion and is an important neurotransmitter for nonadrenergic, noncholinergic neurons. This chapter emphasizes the formation of NO, the technical aspects of its measurement, and its role in the pathobiology of asthma and chronic obstructive pulmonary disease (COPD). NO generated in the lung can directly propagate the epithelial damage that characterizes severe asthma and other airway diseases. Within the lung, NO is a mediator of inflammatory phenomena as it has the ability to influence the phenotype of inflammatory cells, and it contributes to the formation of reactive nitrogen products. Asthmatic individuals have higher exhaled NO concentrations than those encountered in normal individuals. Exhaled NO is used extensively to monitor the effect of corticosteroid treatment in asthma and asthma exacerbations, both spontaneous and induced by steroid reduction.
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