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University of British Columbia Pulmonary Research Laboratory, St. Paul's Hospital, Vancouver, British Columbia, Canada V6Z 1Y6; and Departments of Physiology and Biophysics and of Medicine, University of Washington, Seattle, Washington 98195
Received 17 June 1996; accepted in final form 12 December 1996.
Tsang, John Y. C., Michael J. Emery, and Michael P. Hlastala. Ventilation inhomogeneity in oleic acid-induced
pulmonary edema. J. Appl. Physiol.
82(4): 1040-1045, 1997.
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 (VI) can be quantitatively
partitioned into two components, i.e., convective-dependent inhomogeneity (cdi) and diffusive-convective-dependent inhomogeneity (dcdi). Changes in VI, as represented by the normalized slope of the
phase III alveolar plateau, were studied for 120 min in five
anesthetized mongrel dogs that 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
t = 0. MBHWs were done in
duplicate for 18 breaths every 40 min afterward. Three other dogs that
received only normal saline served as controls. The data show that,
after oleic acid infusion, dcdi, which represents VI in peripheral
airways, is responsible for the increasing total VI as lung water
accumulates progressively over time. The cdi, which represents VI
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 by decreases in ventilation through collateral channels.
convective-dependent inhomogeneity; diffusive-convective-dependent inhomogeneity; diffusion front; extravascular lung water; multiple-breath helium washout technique; phase III alveolar plateau
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