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These predictions built on work from a previous group who had also derived equations to
model NO interactions in the lung (Hyde, Geigel et al. 1997). Their model was able to predict
NO results from the lower airway using a one compartment model but was unable to account
for the upper airway contamination. A later group also used a two compartment model and
reported that a breath hold of 10 to 20 seconds meant that the concentration of NO was
equilibrated - "alveolar airway" production of NO now equaled the amount of NO diffusing
out of the airways (pietropaoli, perillo et al. 1999). The subsequent exhalation could then give
the alveolar content of No. Finally, using similarly derived equations, another group re-
analysed their earlier data, from which they had concluded that NO levels correlated with
expiratory flow (Silkoff, Sylvester et al. 2000). They determined that a even closer
relationship existed between the exhaled No concentration (defined as the quantity of No
exhaled per unit time) and the expiratory flow. They felt this allowed a better estimation of
the quantity of NO diffusing into the exhaled gas and therefore better reflected tissue NO
concentration.
In essence, I believe these groups were making the point that studies were presenting No
results in a far too simplistic manner. NO was being presented as a single result from a single
compartment when in reality the NO concentration varied in different parts of the airway
system. In addition, the levels were always interpreted as if the NO was solely the result of
NO production, while in reality the NO reading was a combination of production' diffusion
(dictated by the rate of removal by capillary blood throughout the lung) and ventilation' The
importance of the modeling described above was to define specifically that different
expiratory rates would allow evaluation of different lung compartments. This could be critical
in appropriately discerning inflammation in different diseases; for example the conducting
airways in the airway disease of asthma or the alveolar compartment in alveolar diseases such
as in interstitial lung disease. This theory was tested by measuring 'fractionated' NO in a
cross section of subjects using three exhalation flows at 100, 1?5 and 370m1/s in 40 newly
diagnosed, steroid naive asthmatics, 17 patients with allergic alveolitis and 57 healthy
controls (Lehrimaki, Kankaanranta et al. 2001). The asthmatic patients did indeed have higher
bronchial NO output at 25nLJs compared to those with alveolitis or healthy controls which
were both measured at 0.7n[./s. On the other hand, the subjects with alveolitis had higher
alveolar NO concentrations at 4.1ppb than the asthmatic or healthy subjects which were both
measured at l.lppb. Thus there was no difference in No between those with asthma and
healthy controls when the alveolar compartment was measured (I-ehtimaki, Kankaanranta et
al. 2001). Finally they demonstrated that the concentration of NO in the bronchial
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