Potential toxic effects of inhaled NO

Inhaled NO may react in the bronchial tree with either O 2 or superoxide (O2-) to produce agents that are potentially toxic for the lung (Gaston, etjaL 1994). The reaction of NO with O2 (at FiO2 = 0.21) to produce NO2 is relatively slow. However, in therapeutic settings and in ventilated patients requiring FiO 2 close to 1, NO conversion to toxic NOx occurs very rapidly (1 s) and it is even quicker in the presence of humidified gas. NO also reacts rapidly with O 2-, which is present at high levels in acute lung injury, to form the peroxynitrite anion (OONO-). At high fractions, NOx and the peroxynitrite anion are toxic to the lung. At low fractions, recent evidence shows that peroxynitrite anion may play a role in defending the lung against microbial invasion.

During inhalation, the NO that reaches blood binds hemoglobin and produces methemoglobin. The balance between oxidation and reduction of methemoglobin results in a blood level of less than 3 per cent in normal subjects. It should be remembered that, in patients with congenital methemoglobinemia, 10 to 20 per cent of methemoglobin is tolerated without ill effects.

Potential toxic effects in patients treated with inhaled NO were recently investigated by increasing fractions of inhaled NO (100-5000 ppm) in patients with acute respiratory distress syndrome. It was shown that, for the highest fraction of NO, although FiO 2 was 1.0, the intratracheal fraction of inhaled NO 2 was 100 ppb and methemoglobin concentrations always remained below 1.4 per cent. In our experience, in 250 patients treated with inhaled NO (5-15 ppm) the measured NO 2 fraction was always 1 to 2 ppm and the methemoglobin concentration was below 2.5 per cent. Thus it can be concluded that, in patients treated with inhaled NO at doses below 15 ppm, NO2 and methemoglobin are usually much below toxic levels.

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