Influence of Bronchomotor Tone on Maximal Expiratory Flow Rates

1970 ◽  
Vol 38 (3) ◽  
pp. 18P-19P
Author(s):  
A. J. S. Gardiner ◽  
L. Wood ◽  
P. Gayrard ◽  
H. Menkes ◽  
P. T. Macklem
CHEST Journal ◽  
1992 ◽  
Vol 102 (5) ◽  
pp. 1636-1637
Author(s):  
Sema Umut ◽  
Bilun Gemicioğlu ◽  
Nurhayat Yildirim

1976 ◽  
Vol 51 (2) ◽  
pp. 133-139
Author(s):  
J. J. Wellman ◽  
E. R. McFadden ◽  
R. H. Ingram

1. Gas-density-dependence of maximal expiratory flow rates (V̇max), defined as the ratio of V̇max while breathing helium/oxygen (80:20) to V̇max. while breathing air at the same lung volume, was examined in relation to other measurements of airways obstruction in patients with obstructive airways disease before and after administration of bronchodilators. 2. Seventeen patients showed a 45% or greater increase in specific conductance(sGaw) after bronchodilator therapy (group A) and thirteen patients demonstrated a lesser response (group B). 3. Before the administration of bronchodilators, the degree of obstruction in the two groups was not different as measured by lung volumes, sGaw, forced expiratory volume in 1 s, and flow rates high in the vital capacity; yet the maximal mid-expiratory flow rate and the degree of density-dependence were significantly lower in group B. 4. After bronchodilators, both groups of patients showed significant improvements in sGaw flow rates and lung volumes. However, group A patients showed a significant increase in density-dependence whereas group B patients did not. 5. Increased density-dependence after bronchodilators in the group A patients was associated with an increase in the computed resistance of the upstream segment with air and a decrease in resistance with helium/oxygen. These changes could be explained by a more mouthward movement of equal pressure points, and therefore a further increase in the relative contribution of the larger density-dependent airways to limitation of flow. 6. The fact that density-dependence was not altered after bronchodilators in the group B patients suggests that the site of limitation of flow did not change appreciably. The shift in the pressure—flow curve for the upstream airways was such that the computed resistance of these airways fell. Thus it appears that the airways comprising the upstream segment were dilated.


1976 ◽  
Vol 41 (2) ◽  
pp. 153-158 ◽  
Author(s):  
J. J. Wellman ◽  
R. Brown ◽  
R. H. Ingram ◽  
J. Mead ◽  
E. R. McFadden

In normal subjects, the second of two successive partial expiratory flow-volume (PEFV 2) curves often had higher isovolume maximal expiratory flow rates (Vmax) than the first (PEFV 1) (mean increase 30.2 +/- 13%). The higher Vmax on PEFV 2 was present only when there was a greater lung elastic recoil pressure (Pst(L)). In eight subjects the Pst(L) derived from sequential partial quasi-static pressure-volume curves, from interruption of the flow-volume maneuvers and at the start of the PEFV curves showed that isovolume upstream resistance increased although Vmax also increased after going to residual volume (RV). In four subjects the RV volume history did not change the pressure flow relationship across the upstream airways. If airways dimensions were the sole determinant of Vmax, then Vmax on PEFV 2 would be the same or smaller than on PEFV 1. That the opposite was observed in our study indicates that the increase in Pst(L), which results from parenchymal hysteresis, offsets any dimensional decrease in upstream airways due to airways hysteresis.


1974 ◽  
Vol 36 (5) ◽  
pp. 554-560 ◽  
Author(s):  
A. J. Gardiner ◽  
L. Wood ◽  
P. Gayrard ◽  
H. Menkes ◽  
P. Macklem

1986 ◽  
Vol 70 (4) ◽  
pp. 347-352 ◽  
Author(s):  
K. E. Berkin ◽  
G. C. Inglis ◽  
S. G. Ball ◽  
N. C. Thomson

1. Airway, cardiovascular and metabolic responses were measured in six asthmatic patients with stable asthma during separate adrenaline, noradrenaline and control infusions. Four incremental infusion rates (4, 10, 25 and 62.5 ng min−1 kg−1) produced circulating catecholamine concentrations within the physiological range. 2. Specific airways conductance and maximal expiratory flow rates measured from complete and partial flow-volume curves increased significantly (P < 0.05) during adrenaline infusion, in a dose-response manner. 3. No changes in specific airways conductance or maximal expiratory flow rates were seen during the noradrenaline or control infusion. 4. The highest adrenaline infusion rate caused a rise in systolic blood pressure (P < 0.05) and plasma glucose (P < 0.05) and a fall in plasma potassium (P < 0.05). 5. Noradrenaline infusion caused a slight increase in diastolic blood pressure (P < 0.05) but no metabolic changes. No cardiovascular or metabolic changes occurred during the control infusion. 6. Infused adrenaline, producing circulating concentrations within the physiological range, caused dose-related bronchodilatation in asthmatic patients. Circulating noradrenaline does not appear to have a role in the control of basal airway tone in asthmatic patients.


CHEST Journal ◽  
1979 ◽  
Vol 76 (1) ◽  
pp. 59-63 ◽  
Author(s):  
Dan Stanescu ◽  
Claude Veriter ◽  
René Van Leemputten ◽  
Lucien Brasseur

1995 ◽  
Vol 78 (4) ◽  
pp. 1421-1424 ◽  
Author(s):  
E. Thorsen ◽  
B. K. Kambestad

To assess the contribution of hyperoxia to reduced pulmonary function after a deep saturation dive, a shallow saturation dive to a pressure of 0.25 MPa with the same profile of hyperoxic exposure as in a deep saturation dive to 3.7 MPa was conducted. The PO2 was 40 kPa, with periods of 75 kPa for 2 h every 2nd day during the first 14 days, 50 kPa the next 12 days, and a gradual fall to 21 kPa over the last 2 days in decompression. Seven submariners and one professional diver aged 22–27 yr participated. Pulmonary function, including static and dynamic lung volumes and flows and transfer factor for carbon monoxide (TLCO), were measured twice before, immediately after, 1 mo after, and 1 and 3 yr after the dive. As reported previously, there was a significant reduction in TLCO and in maximal expiratory flow rates at low lung volumes immediately after the dive. At the follow-up examinations 1 and 3 yr after, there was no recovery of the maximal expiratory flow rates. Forced midexpiratory flow rate was still reduced by 8.7 +/- 5.6% (P < 0.05) and 9.3 +/- 7.1% (P < 0.01), respectively. Forced expired volume in 1 s and forced vital capacity were not significantly reduced. There was a complete recovery of the TLCO. The findings are consistent with the studies indicating development of airway obstruction in divers, and the findings indicate that exposure to hyperoxia contributes to this effect.


1998 ◽  
Vol 84 (6) ◽  
pp. 1872-1881 ◽  
Author(s):  
Steven R. McClaran ◽  
Craig A. Harms ◽  
David F. Pegelow ◽  
Jerome A. Dempsey

We subjected 29 healthy young women (age: 27 ± 1 yr) with a wide range of fitness levels [maximal oxygen uptake (V˙o 2 max): 57 ± 6 ml ⋅ kg−1 ⋅ min−1; 35–70 ml ⋅ kg−1 ⋅ min−1] to a progressive treadmill running test. Our subjects had significantly smaller lung volumes and lower maximal expiratory flow rates, irrespective of fitness level, compared with predicted values for age- and height-matched men. The higher maximal workload in highly fit (V˙o 2 max > 57 ml ⋅ kg−1 ⋅ min−1, n = 14) vs. less-fit (V˙o 2 max < 56 ml ⋅ kg−1 ⋅ min−1, n = 15) women caused a higher maximal ventilation (V˙e) with increased tidal volume (Vt) and breathing frequency (fb) at comparable maximal Vt/vital capacity (VC). More expiratory flow limitation (EFL; 22 ± 4% of Vt) was also observed during heavy exercise in highly fit vs. less-fit women, causing higher end-expiratory and end-inspiratory lung volumes and greater usage of their maximum available ventilatory reserves. HeO2 (79% He-21% O2) vs. room air exercise trials were compared (with screens added to equalize external apparatus resistance). HeO2 increased maximal expiratory flow rates (20–38%) throughout the range of VC, which significantly reduced EFL during heavy exercise. When EFL was reduced with HeO2, Vt, fb, andV˙e (+16 ± 2 l/min) were significantly increased during maximal exercise. However, in the absence of EFL (during room air exercise), HeO2 had no effect onV˙e. We conclude that smaller lung volumes and maximal flow rates for women in general, and especially highly fit women, caused increased prevalence of EFL during heavy exercise, a relative hyperinflation, an increased reliance on fb, and a greater encroachment on the ventilatory “reserve.” Consequently, Vt andV˙e are mechanically constrained during maximal exercise in many fit women because the demand for high expiratory flow rates encroaches on the airways’ maximum flow-volume envelope.


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