Bypassing nasal NO

NO has been shown to be a potent vasodilator. When given by inhalation it dilates pulmonary vessels selectively; the systemic circulation is unaffected because of the binding of NO to hemoglobin. NO can be measured in expired gas as an indication of endogenous production in the lung. Only small amounts of NO are expired from the lower airways (2-4 ppb) and most seems to come from the nose. Very high concentrations (around 9000 ppb) have been measured in the paranasal sinuses, which also seem to be the source of NO that is measured in the nose. Whether nasal NO is part of the immunodefense system or whether it modulates ventilation-perfusion matching via autoinhalation is a subject of discussion. Recently, arterial oxygenation has been shown to improve in patients mechanically ventilated for neurological disorders when NO is added to the inspired gas ( Lundbergefa/., 19,95). These patients were considered to have essentially healthy lungs;

however, an effect of 'autoinhaled' NO was still seen. This supports the hypothesis that nasal NO has a role in the regulation of ventilation-perfusion matching. If this is true, intubation of the trachea eliminates the potentially beneficial effect of nasal NO and may require replacement therapy. However, NO concentrations are extremely small, well below those used for inhalational NO treatment in acute respiratory failure ( Lundberg.etal 19,9.5).

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