scholarly journals Simultaneous measurement of nitric oxide production by conducting and alveolar airways of humans

1999 ◽  
Vol 87 (4) ◽  
pp. 1532-1542 ◽  
Author(s):  
Anthony P. Pietropaoli ◽  
Irene B. Perillo ◽  
Alfonso Torres ◽  
Peter T. Perkins ◽  
Lauren M. Frasier ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Normal Subjects ◽  
Breath Holding ◽  
No Production ◽  
Large Contribution ◽  
Flow Rates ◽  
Expiratory Flow ◽  
Human Airways ◽  
Conducting Airways ◽  
Expiratory Flow Rates

Human airways produce nitric oxide (NO), and exhaled NO increases as expiratory flow rates fall. We show that mixing during exhalation between the NO produced by the lower, alveolar airways (V˙l NO) and the upper conducting airways (V˙u NO) explains this phenomenon and permits measurement ofV˙l NO,V˙u NO, and the NO diffusing capacity of the conducting airways (Du NO). After breath holding for 10–15 s the partial pressure of alveolar NO (Pa) becomes constant, and during a subsequent exhalation at a constant expiratory flow rate the alveoli will deliver a stable amount of NO to the conducting airways. The conducting airways secrete NO into the lumen (V˙u NO), which mixes with Pa during exhalation, resulting in the observed expiratory concentration of NO (Pe). At fast exhalations, Pa makes a large contribution to Pe, and, at slow exhalations, NO from the conducting airways predominates. Simple equations describing this mixing, combined with measurements of Pe at several different expiratory flow rates, permit calculation of Pa,V˙u NO, and Du NO.V˙l NOis the product of Pa and the alveolar airway diffusion capacity for NO. In seven normal subjects, Pa = 1.6 ± 0.7 × 10−6 (SD) Torr,V˙l NO= 0.19 ± 0.07 μl/min,V˙u NO= 0.08 ± 0.05 μl/min, and Du NO = 0.4 ± 0.4 ml ⋅ min−1 ⋅ Torr−1. These quantitative measurements ofV˙l NOandV˙u NOare suitable for exploring alterations in NO production at these sites by diseases and physiological stresses.

Breathing at low lung volumes and chest strapping: a comparison of lung mechanics

1981 ◽  
Vol 50 (3) ◽  
pp. 650-657 ◽  
Author(s):  
N. J. Douglas ◽  
G. B. Drummond ◽  
M. F. Sudlow
Keyword(s):  
Lung Volume ◽  
Maximum Flow ◽  
Normal Subjects ◽  
Lung Mechanics ◽  
Lung Volumes ◽  
Flow Rates ◽  
Recoil Pressure ◽  
Forced Expiratory Flow ◽  
Expiratory Flow ◽  
Expiratory Flow Rates

In six normal subjects forced expiratory flow rates increased progressively with increasing degrees of chest strapping. In nine normal subjects forced expiratory flow rates increased with the time spent breathing with expiratory reserve volume 0.5 liters above residual volume, the increase being significant by 30 s (P less than 0.01), and flow rates were still increasing at 2 min, the longest time the subjects could breathe at this lung volume. The increase in flow after low lung volume breathing (LLVB) was similar to that produced by strapping. The effect of LLVB was diminished by the inhalation of the atropinelike drug ipratropium. Quasistatic recoil pressures were higher following strapping and LLVB than on partial or maximal expiration, but the rise in recoil pressure was insufficient to account for all the observed increased in maximum flow. We suggest that the effects of chest strapping are due to LLVB and that both cause bronchodilatation.

Effect of volume history on successive partial expiratory flow-volume maneuvers

1976 ◽  
Vol 41 (2) ◽  
pp. 153-158 ◽  
Author(s):  
J. J. Wellman ◽  
R. Brown ◽  
R. H. Ingram ◽  
J. Mead ◽  
E. R. McFadden
Keyword(s):  
Static Pressure ◽  
Normal Subjects ◽  
Flow Volume ◽  
Elastic Recoil ◽  
Flow Rates ◽  
Recoil Pressure ◽  
Maximal Expiratory Flow ◽  
Expiratory Flow ◽  
Expiratory Flow Rates ◽  
Volume History

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.

Influence of expiratory flow on closing capacity at low expiratory flow rates

1975 ◽  
Vol 39 (1) ◽  
pp. 60-65 ◽  
Author(s):  
J. R. Rodarte ◽  
R. E. Hyatt ◽  
D. A. Cortese
Keyword(s):  
Lung Volume ◽  
Normal Subjects ◽  
Closing Volume ◽  
Residual Volume ◽  
Dependent Lung ◽  
Flow Rates ◽  
Single Breath ◽  
Expiratory Flow ◽  
Expiratory Flow Rates ◽  
Phase Iv

Single-breath oxygen (SBO2) tests at expiratory flow rates of 0.2, 0.5, and 1.01/s were performed by 10 normal subjects in a body plethysmograph. Closing capacity (CC)--the absolute lung volume at which phase IV began--increased significantly with increases in flow. Five subjects were restudied with a 200-ml bolus of 100% N2 inspired from residual volume after N2 washout by breathing 100% O2 and similar results were obtained. An additional five subjects performed SBO2 tests in the standing, supine, and prone positions; closing volume (CV)--the lung volume above residual volume at which phase IV began--also increased with increases of expiratory flow. The observed increase in CC with increasing flow did not appear to result from dependent lung regions reaching some critical “closing volume” at a higher overall lung volume. In normal subjects, the phase IV increase in NI concentration may be caused by the asynchronous onset of flow limitation occurring initially in dependent regions.

Role of the parasympathetic nervous system in acute lung response to ozone

1985 ◽  
Vol 59 (6) ◽  
pp. 1879-1885 ◽  
Author(s):  
W. S. Beckett ◽  
W. F. McDonnell ◽  
D. H. Horstman ◽  
D. E. House
Keyword(s):  
Nervous System ◽  
Airway Resistance ◽  
Parasympathetic Nervous System ◽  
Normal Subjects ◽  
Lung Mechanics ◽  
Flow Rates ◽  
Forced Expiratory Flow ◽  
Expiratory Flow ◽  
Expiratory Flow Rates

We conducted an ozone (O3) exposure study using atropine, a muscarinic receptor blocker, to determine the role of the parasympathetic nervous system in the acute response to O3. Eight normal subjects with predetermined O3 responsiveness were randomly assigned an order for four experimental exposures. For each exposure a subject inhaled either buffered saline or atropine aerosol followed by exposure either to clean air or 0.4 ppm O3. Measurements of lung mechanics, ventilatory response to exercise, and symptoms were obtained before and after exposure. O3 exposure alone resulted in significant changes in specific airway resistance, forced vital capacity (FVC), forced expiratory flow rates, tidal volume (VT), and respiratory rate (f). Atropine pretreatment prevented the significant increase in airway resistance with O3 exposure and partially blocked the decrease in forced expiratory flow rates but did not prevent a significant fall in FVC, changes in f and VT, or the frequency of reported respiratory symptoms after O3. These results suggest that the increase in pulmonary resistance during O3 exposure is mediated by a parasympathetic mechanism and that changes in other measured variables are mediated, at least partially, by mechanisms not dependent on muscarinic cholinergic receptors of the parasympathetic nervous system.

Measurement of peak expiratory flow rates in 220 normal children from 4.5 to 18.5 years of age

1963 ◽  
Vol 62 (2) ◽  
pp. 186-189 ◽  
Author(s):  
Andrew B. Murray ◽  
Charles D. Cook ◽  
Joanna H. Shaw ◽  
Mary Alice Shahidi
Keyword(s):  
Peak Expiratory Flow ◽  
Normal Children ◽  
Flow Rates ◽  
Expiratory Flow ◽  
Expiratory Flow Rates

Patterns of gas flow in the upper bronchial tree

1959 ◽  
Vol 14 (5) ◽  
pp. 753-759 ◽  
Author(s):  
J. B. West ◽  
P. Hugh-Jones
Keyword(s):  
Gas Flow ◽  
Lower Lobe ◽  
Bronchial Tree ◽  
High Flow ◽  
Human Beings ◽  
Lobe Bronchus ◽  
Flow Rates ◽  
Expiratory Flow ◽  
Different Gases ◽  
Expiratory Flow Rates

Patterns of gas flow in the upper bronchial tree have been studied by observing the flow of dye and different gases through a lung cast, and by measurements made on open-chested dogs and on human beings at bronchoscopy. Flow is completely laminar throughout the bronchial tree at low expiratory flow rates (up to 10 l/min.) and completely turbulent, proximal to the segmental bronchi, at high flow rates (80 l/min.). Both at low and high expiratory flow rates, gas from segmental bronchi was not uniformly mixed in the lobar or main bronchi which they supplied. The composition of a catheter sample in these airways would therefore not be representative of the alveolar gas in the corresponding lobe or lung unless the alveolar gas in all areas distal to the sampling tube was homogeneous. Penetration of the left upper lobe bronchus by gas from the lower lobe was demonstrated in the model and a normal subject at bronchoscopy. Submitted on September 3, 1958

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