Inhaled nitric oxide (NO) is used to treat various cardiopulmonary disorder
s associated with pulmonary hypertension. The rationale is based on the fac
t that NO, given by inhalation, only dilates those pulmonary vessels that p
erfuse well-ventilated lung units. As a result, pulmonary gas exchange is i
mproved while pulmonary vascular resistance is reduced and pulmonary blood
flow is increased. Inhaled NO has been succesfully applied to treat persist
ent pulmonary hypertension of the newborn, reducing the need for extracorpo
real life support. Although pulmonary hypertension and altered vasoreactivi
ty contribute to profound hypoxaemia in adult and paediatric acute respirat
ory distress syndrome (ARDS), the benefit of inhaled NO still remains to be
established in patients with ARDS. ARDS is a complex response of the lung
to direct or indirect insults, leading to pulmonary vasoconstriction and va
rious inflammatory responses. Recent randomized trials suggest that inhaled
NO only causes a transient improvement in oxygenation. Whether this effect
is important in the long-term management of ARDS remains to be established
. NO, measured in the exhaled breath, is an elegant and non-invasive means
to monitor inflammation of the upper and lower respiratory tract. In the no
rmal upper airways, the bulk of exhaled NO originates from the paranasal si
nuses. Exhaled NO is increased in nasal allergy and decreased in cystic fib
rosis, nasal polyposis and chronic sinusitis. That NO production is increas
ed in asthmatic airways is also well established. However, several question
s still need to be addressed, in particular evaluation of the sensitivity a
nd specificity of the measurement techniques, and assessment of the broncho
dilator action of endogenous NO.