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al found levels of 10.3ppb compared to controls at 8.4ppb, Massaro et al found levels of
13.2ppb compared to controls at 4.7ppb, and Robbins et al found levels of 174ppb compared
to controls of 105.5ppb (Kharitonov, Yates et al. 1994; Persson, Zetterstrom et al. 1994;
Massaro, Mehta et al. 1996; Robbins, Floreani et al. 1996). Alving et al demonstrated no
overlap between their control group with a range of 5-16ppb and their asthmatic group who
had a range measured at 2I-3Ippb (Alving, Weitzberg et al. 1993). Massaro demonstrated
that the NO levels were even higher during a period of acute asthma in seven patients
requiring emergency department treatment with a reduction of NO beginning by 48 hours
(Massaro, Gaston et al. 1995) and Kharitinov et al showed a reduction over three weeks in
eleven asthmatic patients who commenced on IHCS therapy. However, as can be seen above,
the absolute mean concentrations of exhaled NO obtained by these separate workers in similar
patient groups and normal subjects using similar techniques appeared so disparate as to be
confusing.
In addition, the regional source of NO within the respiratory tract was debated. Initially
Borland et al suggested that the NO measured in exhaled air from a single full exhalation and
during tidal breathing was of alveolar origin like COz (Borland, Cox et al. 1993). Persson et al
then suggested that NO was formed preferentially in the small airways such as the terminal
and respiratory bronchioles (Persson, Wiklund et al. 1993). By comparing the concentrations
of NO exhaled during tidal breathing through either nose or mouth, Alving et al suggested
that the major contribution came from the nasal space with a minor addition from the lower
airways (Alving, Weitzberg et al. 1993). Lundberg et al demonstrated a decreasing
concentration of exhaled NO when sampling progressively down the respiratory tract at the
nose, mouth and, in four tracheotomised patients, below the vocal cords (Lundberg, Farkas-
Szallasi et al. 1995).
Another goup also looked at exhaled concentrations of NO in five adults with tracheostomy
during spontaneous breathing where oral NO concentrations were 9 - 25.7ppb while via the
tracheostomy this dropped to l.l - 6.5ppb. Eleven patients admitted for minor abdominal
surgery had similar decreases in NO levels measured under anaesthesia from nasal (mean
54ppb), oral (mean l3ppb) and following intubation (mean 1.3ppb, which was close to the
lower detection limit of their analyser). Seven patients intubated and ventilated in intensive
care with multiple diagnoses all had NO concentration levels close to the detection limit of the
analyser (range of 0.0 - 1.3ppb) (Schedin, Frostell et al. 1995). By isolating the nasal passages
from the rest of the respiratory tract with voluntary closure of the soft palate, Kimberly et al
showed the release of NO in the nasal passages was approximately seven times greater than
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