Ventilation inhomogeneity in oleic acid induced pulmonary
edema.
Tsang, John Y. C., Michael J. Emery, and Michael P. Hlastala.
UBC Pulmonary Research Laboratory, St. Paul's Hospital, 1081
Burrard Street, Vancouver, B.C., Canada V6Z 1Y6, Departments of
Physiology & Biophysics and of Medicine, University of
Washington, Seattle, WA 98195
APStracts 3:0578A, 1996.
Oleic acid causes permeability pulmonary edema in the lung, resulting
in impairment of gas exchange and ventilation perfusion heterogeneity
and mismatch. Previous studies have shown that by using the multiple
breath helium washout (MBHW) technique, ventilation inhomogeneity
(V.I.) can be quantitatively partitioned into two components, i.e.,
convective dependent inhomogeneity (cdi) and diffusive-convective
dependent inhomogeneity (dcdi). Changes in V.I., as represented by
the normalized slope of the phase III alveolar plateau, were studied
for 120 minutes in 5 anaesthetized mongrel dogs which were ventilated
under paralysis by a constant flow linear motor ventilator. These
animals received oleic acid (0.1 mg/Kg) infusion into the right
atrium at time = 0 minutes. MBHW's were done in duplicate for 18
breaths every 40 minutes afterwards. Three other dogs which received
only normal saline served as controls. The data show that after oleic
acid infusion, dcdi which represents V.I. in peripheral airways is
responsible for the increasing total V.I. as lung water accumulates
progressively over time. Cdi, which represents V.I. between larger
conductive airways remains relatively constant throughout. This
observation can be explained by increases in the heterogeneity of
tissue compliance in the periphery, distal airway closure or
decreases in ventilation through collateral channels.
Received 17 June 1996; accepted in final form 12 December 1996.
APS Manuscript Number A557-6.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996