Journal of Applied Physiology, Vol 68, Issue 5 2006-2012, Copyright © 1990 by American Physiological Society
Insensitivity of maximum expiratory flow to bronchodilation in normal dogs
J. Eng, A. Gomez and S. Mink
Section of Respiratory Diseases, University of Manitoba, Winnipeg, Canada.
We examined the effects of the inhaled parasympatholytic agent atropine and
the sympathomimetic agent salbutamol on partitioned frictional pressure
(Pfr) losses to the site of flow limitation (choke point, CP) in dogs to
see how changes brought about by these agents would affect maximum
expiratory flow (Vmax) and response to breathing 80% He-20% O2 (delta Vmax)
in terms of wave-speed theory of flow limitation. In open-chest dogs, a
Pitot-static tube was advanced down the right lower lobe to locate CP, to
determine CP lateral and end-on pressures (PE), and to partition the airway
into peripheral (alveoli to sublobar) and central (sublobar to CP)
segments. Measurements were obtained at approximately 50% vital capacity.
After inhalation, CP locations were unchanged with both bronchodilating
agents. After atropine inhalation, Pfr central was decreased by one-half
compared with base line. Despite the decrease in Pfr central, however, Vmax
failed to increase after atropine because of altered bronchial area
pressure (BAP) behavior at the CP site. After salbutamol inhalation, Pfr
peripheral was reduced by about one-half compared with base line. However,
Vmax failed to increase, because this reduction was too small to
significantly increase the CP pressure head (i.e., PE). delta Vmax was also
insensitive to these agents. Our results show mechanisms by which small
changes in Pfr, as well as the complex interaction of changes in Pfr and
BAP, may limit the use of Vmax in detecting bronchodilation at different
airway sites.
