EFFECT OF LUNG-VOLUME AND INTRATHORACIC PRESSURE ON AIRWAY MUCOSAL BLOOD-FLOW IN MAN

We have recently described an inert soluble gas uptake technique (usin g dimethyl-ether, DME) for the non-invasive measurement of airway muco sal blood flow (Q(aw)) in humans, In the present study, we assessed th e effects of lung volume and intrathoracic pressure on Q(aw), in healt hy non-smokers (age range 19-52 years). Q(aw) was calculated from the steady-state uptake of DME from a 50 ml segment of the anatomic dead s pace. The mean (+/- SD) Q(aw) of three consecutive measurements at a l ung 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 air way pressure, there was an inverse relationship between apparent Q(aw) on the one hand and lung volume and anatomic dead space (DS) on the o ther: mean Q(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 TLC (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(2)O (modified Valsalva maneuver) d ecreased mean Q(aw) to 3.3 +/- 2.8 ml.min(-1) while a decrease in intr athoracic pressure to -35 cmH(2)O (modified Muller maneuver) increased mean Q(aw) to 17.1 +/- 7.4 ml.min(-1) from a control value of 7.2 +/- 2.2 ml.min(-1) (n = 7; P< 0.05 among all three). These results indica te that lung volume has an effect on apparent Q(aw), presumably by inf luencing the depth to which the analyzed anatomical dead space segment extends into the bronchial tree. The results also show that changes i n intrathoracic pressure alter Q(aw), possibly reflecting concomitant changes in left ventricular output and its distribution to intrathorac ic and extrathoracic vascular beds.