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higher level of exhaled NO at 4.9ppb (+l-2.6ppb) than the controls but this did not reach
significance. They also found no conelation between NO and the lung function in any goup
@otsch, Demirakca et al. 1996). In another study, Grasemann et al measured NO by single
exhalations to an analyser that had a 10 second response time across a wide age range of
subjects (Grasemann, Michler et al.1997). The mean exhaled NO level in 30 control subjects
aged six to 37 years was 9.1 ppb (+/- 3.6ppb) which was significantly lower in 27 subjects
with CF aged six to 40 years at a time of disease stability at 5.9ppb (+l- 2.6ppb). This goup
commented that : "In preliminary experiments we observed that the higher NO concentrations
in ambient air were associated with increased exhaled NO concentrations." In view of this,
they went on to calculate the difference between the NO levels taking into account this
ambient NO concentration and still found a significant difference with the control group
having levels of 5.0ppb (+f3.lppb) compared to the CF group at 1.5ppb (+/- l.2ppb)
(Grasemann, Michler et al. 1997). Finally Balfour-Lynn et al measured plateau exhaled NO at
the time of COz plateau by placing a plastic nose piece just inside one nostril which was then
connected to the Teflon tubing of the NO analyser. They showed a significant difference
between the nasal measurements from 57 control children at l024ppb (95Vo CI896-1l52ppb)
when compared to children with CF; in thirteen on IHCS at 522ppb (95Vo CI313-730ppb) or
50 not on IHCS at 460ppb (95Vo C[399-520ppb). There was no difference in the exhaled NO
levels in these two groups and the use of IHCS did not affect the exhaled oral levels of NO in
the CF group with the results being means of 4.8ppb (95Vo Cl3.8-5.8ppb) in control children,
4.7ppb (957o Cl4.0-5.3ppb) in those with CF not on steroids and 3.6ppb (957o Cl2.5-4.8ppb)
in CF children on steroids. There was also no significant difference in the NO levels in the CF
goup between those 26 colonised with Pseudomonas aeruginosa compared to the 24 non-
colonised. There did appear to be a difference with a lower level in those 31 colonised with
Staphyloccocal aureus at a mean of 4ppb (95Vo CI3.44.6ppb) and those 19 which did not
have this organism at 5.8ppb (95Vo CI 4.4-7.2ppb). As there were 63 children in total there
must have been some considerable overlap between having Staphylococcal aureus and/or
Pseudomonas aeruginosa, plus the correct identification of the true presence of lower
respiratory tract pathogens in this age group with CF is known to be difficult so the overlaps
within these groups may have obscured findings (Balfour-Lynn, Laverty et al. 1996).
This completed my work in this area. I had demonstrated some key findings of factors that
affected exhaled NO measurements and would require standardisation for procedures in the
future. These were expiratory flow, expiratory mouth pressure, the need for low ambient NO
levels or to inhale from a reservoir of NO free air, and the need to prevent water consumption
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