Nitric Oxide and the Respiratory System

Work with NO and the respiratory system provides the only direct evidence of NO production in vivo in humans, and analytical techniques devised for the detection of NO as an atmospheric pollutant have been applied. Reaction between NO and ozone leads to the generation of light (equations 5 and 6). 

A variety of chemiluminescence analysers is now available for quantitation of NO, and such equipment can be adapted readily for routine measurement of endogenous NO excreted in expired air. The technique is highly sensitive (detection limit 1 ppb) and linear over a wide range 1 to 1000 ppb can easily be covered without recalibration of equipment. Analyses are rapid and highly reproducible. Further work is still required to establish the exact origins of NO contributing to exhalation profiles recorded with this technology. Both lower and upper respiratory tracts release NO into expirate.  

NO is able to cause vascular and bronchial smooth muscle relaxation. The principal mode of action is stimulation of soluble guanylate cyclase with consequent rises in intracellular cyclic GMP. Inhalation of NO gives selective reduction in pulmonary vascular resistance in pulmonary hypertension and in adult respiratory distress syndrome (ARDS). ° ARDS is a severe and often fatal condition associated with pulmonary oedema and reduced right ventricular function. It is often treated with vasodilators to reduce pulmonary artery press- 

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