Zusammenfassung
Wir untersuchten mittels verschiedener Atemflüsse, ob sich Unterschiede zwischen Rauchern
und Nichtrauchern hinsichtlich der differenziellen NO-Parameter Bronchialwand-Konzentration
(Caw), alveolare Konzentration (Calv) und Diffusionskoeffizient (DawNO) ergeben. Die 34 untersuchten beschwerdefreien, nicht therapierten Raucher weisen
im Vergleich zu 43 gesunden Nichtrauchern signifikant niedrigere FeNO-Werte auf. Die
Analyse der differenziellen NO-Parameter mittels des 2-Kompartimenten-Modells der
NO-Produktion belegt unter Rauchern eine signifikant verminderte bronchiale NO-Konzentration,
jedoch keine signifikante Änderung der dem Alveolarbereich zugerechneten NO-Fraktion.
Die Zusammenhänge zwischen den einzelnen NO-Parametern der Nichtraucher passen zum
2-Kompartimenten-Modell. Im Gegensatz dazu weisen Raucher eine monotone positive Korrelation
zwischen den verminderten Caw und FeNO unter allen fünf Flussraten auf. Das könnte darauf zurückzuführen sein,
dass das alveolare NO der Raucher teilweise aus dem bronchialen Bereich stammt. Das
passt zu deren signifikant erniedrigten FEV1-, FEF50- und FEF75-Werten, welche mit Turbulenzen und unterschiedlichen Verzögerungen des exspiratorischen
Gasabflusses im Bronchiolo-Alveolarbereich einhergehen. Wir stellen die Hypothese
auf, dass der verminderten NO-Konzentration in der Bronchialwand des Rauchers eine
pathophysiologische Rolle bei der Manifestation eines Small airways disease zukommt.
Abstract
Our aim was to determine by means of five exhaled flow rates differential parameters
of FeNO and the relations between them in smokers and non-smokers. 34 smokers (without
respiratory symptoms and medication) were examined. Compared to 43 healthy non-smokers,
FeNO was significantly lower. The analysis of the differential NO parameters by means
of the two-compartment model of NO production revealed a significant decrease in the
bronchial NO concentration, but no significant changes of NO in alveolar fraction
by smokers. The relations between differential parameters in non-smokers confirm the
theoretical expectations of the two-compartment model. Conversely, smokers exhibit
an abnormal remarkable correlation, namely, a high correlation between the reduced
Caw und FeNO at all five flow rates. It may be assumed that the alveolar NO fraction
in smokers is to some extent of bronchial origin. Such a preposition is in line with
significantly decreases of FEV1, FEF50 and FEF75 in smokers, which are associated with turbulences, flow inhomogeneity and a varied
delay of expiration time from the peripheral airways. We hypothesize that the decreased
NO concentration in the bronchial wall of smokers plays a pathophysiological role
in the genesis of small airways disease.
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Liubov Barbinova
Ordinariat und Zentralinstitut für Arbeitsmedizin und Maritime Medizin Hamburg
Seewartenstraße 10
20459 Hamburg
eMail: lioukov@uke.uni-hamburg.de