Abstract

We have recently described an inert soluble gas uptake technique (using dimethyl-ether, DME) for the non-invasive measurement of airway mucosal blood flow Q̇ aw, in humans. In the present study, we assessed the effects of lung volume and intrathoracic pressure on Q̇ aw, in healthy non-smokers (age range 19–52 years). Q̇ aw was calculated from the steady-uptake of DME from a 50 ml segment of the antomic dead space. The mean (± SD) Q̇ aw of three consecutive measurement at a lung volume of FRC + 300 ml was 8.3 ± 2.3, 8.6±2.6 and 8.3 ± 2.7 ml · min −1 ( n = 13; coefficient of variation 14 ± 7%). At zero airway pressure, there was an inverse relationship between apparent Q̇ aw on the one hand and lung volume and anatomic dead space (DS) on the other: mean Q̇ aw was 12.2 ± 5.3, 8.2 ± 2.5 and 5.3 ± 2.2. ml · min −1 at RV + 300 ml(DS = 131 ± 11 ml), FRC + 300 ml (DS = 153 ± 12 ml) and TCL (DS = 206 ± 22 ml) positions, respectively ( n = 11; P < 0.05 among all three). At a lung volume of FRC + 300 ml, an increase in intrathoracic pressure to +25 cmH 2O (modified Valsalva maneuver) decreased mean Q̇ aw to 3.3 ± 2.8 ml · min −1 while a decrease in intrathoracic pressure to −35 cmH 2O (modified Müller maneuver) increased mean Q̇ aw to 17.1 ± 7.4ml · min −1 from a control value of 7.2 ± 2.2 ml · min · min − ( n = 7; P < 0.05 among all three). These results indicate that lung volume has an effect on apparent Q̇ aw, presumably by influencing the depth to which the analyzed anatomical dead space segment extends into the bronchial tree. The results alos show that changes in intrathoracic pressure alter Q̇ aw possibly reflecting concomitant changes in left ventricular output and its distribution to intrathoracic and extrathoracic vascular beds.

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