Autoinhaled nitric oxide (NO) is produced mainly in the upper airways. Orotracheal intubation disrupts the natural autoinhalation of NO from the naso-and oropharynx. The effect of disrupting and then replacing autoinhaled NO on arterial oxygenation was investigated in intubated patients.Two groups of nine patients without lung disease were examined during anaesthesia using an inspired oxygen fraction of 0.50. In both groups, the individually produced NO of the whole respiratory tract and the upper airways was determined. The amount of NO normally autoinhaled from the upper airways was replaced for 5 min after orotracheal intubation in one group.The amount of NO from the upper respiratory tract was 47¡19 parts per billion (ppb) in the test group and the replaced NO concentration was 48¡20 ppb. No significant increase in arterial oxygen tension could be detected during the replacement of the autoinhaled NO. Haemodynamic parameters remained unchanged. In the control group, the NO from the upper airways was 34¡16 ppb. In contrast to the test group, it was not replaced after intubation.These findings suggest that in healthy subjects the autoinhalation of nitric oxide does not play an important role in arterial oxygenation during anaesthesia. Nitric oxide (NO) is formed within the respiratory tract by the enzyme NO synthase, which converts L-arginine to L-citrulline. NO has several physiological functions. It contributes to the modulation of the pulmonary vascular tone under physiological conditions and, perhaps more importantly, during hypoxia [1]. The major portion of endogenous NO is produced in the upper respiratory tract, particularly in the nasopharynx [2][3][4]. Under physiological conditions the NO produced in the oro-and nasopharynx is inhaled to some extent. Endotracheal intubation disrupts this autoinhalation from the upper airways. It is estimated that y50-100 parts per billion (ppb) are autoinhaled during normal breathing [2,5]. In various diseases associated with pulmonary hypertension, inhalation of exogenous NO in supranormal concentrations is used as a therapeutic means to selectively decrease pulmonary vascular resistance in ventilated lung regions. Therefore, the ventilation/perfusion mismatch and the intrapulmonary right-to-left shunt are reduced, and consequently the arterial oxygenation is improved [6][7][8][9][10]. The physiological implication of autoinhaled NO in healthy humans is still unknown.Bypassing the upper airway by orotracheal intubation disrupts the autoinhalation of NO from the oro-and nasopharynx. Therefore, the authors sought to investigate the physiological role of autoinhaled NO in patients in whom anaesthesia was induced and who were intubated. The hypothesis that the replacement of the exact amount of endogenous NO influences the arterial oxygenation was tested in a randomised, controlled study.
MethodsThe study was approved by the hospital ethics committee and informed consent was obtained from each patient the day prior to the operation.
PatientsThe patients invest...
