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etween these researchers were documented in the literature for other subject groups such as
those with asthma, bronchiectasis, hypertension and smokers. The measurement of NO in
these studies did vary between mean peak exhaled NO, mean plateau exhaled NO and NO
measured during tidal breathing. This led me to the suspicion that the technique of
measurement critically affected the No levels obtained. In the first methodological study in
twelve healthy adults (Byrnes, Dinarevic et al. 1997), I demonstrated that the concentration of
NO obtained could be halved depending on whether the subject was breathing directly into
the No analyser (mean 84.Sppb) or breathing through a t-piece system (mean 41.2ppb)' The
main difference between these two methods was a change in flow from 440 mls/min to 665
mls/min. The methodology experiments detailed in this chapter were therefore designed to
determine what factors altered the concentration of exhaled No obtained.
In the second methodological study, changing the expiratory flow rate significantly altered the
mean concentration of NO obtained. The higher the expiratory flow' the lower the
concentrations recorded, with a mean decrease of 35ppb when moving from 25omls/min to
1100mls/min in ten subjects (see Figure 7.1). Most of the literature at the time in the cross
sectional studies had usually mentioned the samplin g rate of the machine only, or measured
tidal volumes over a L-2 minute time periods with none specifically noting a standard
expiratory flow. Alving et al reported that if the airflow was increased in 12 healthy controls
from2umin-l to 5 Umin-l a slight increase in the levels of No was noted -
the data were not
shown and the increase was noted to be insignificant. This proved a different finding from
most others (Alving 1993). Imada et al showed a hyperbolic relationship between the NO
concentration and the sampling flow rate (see Figure 7'10) with a marked reduction of
exhaled No when increasing flow in one subject (Imada 1996).
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