Affiliation:
1. University of British Columbia Pulmonary Research Laboratory, St. Paul's Hospital, Vancouver, British Columbia, Canada V6Z 1Y6; and
2. Departments of Physiology and Biophysics and Medicine, University of Washington, Seattle, Washington 98195
Abstract
By using the multiple-breath helium washout technique, ventilation heterogeneity (V˙H) after embolic injury in the lung can be quantitatively partitioned into the conductive and acinar components. Total V˙H, represented by the normalized slope of the phase III alveolar plateau, SnIII (total), was studied for 120 min in three groups of anesthetized and paralyzed mongrel dogs. Group 1 ( n = 3) received only normal saline and served as controls. Group 2 ( n = 4) received repeated infusions of polystyrene beads (250 μm) into the right atrium at 10, 40, 80, and 120 min. Group 3 ( n = 3) was similarly treated, except that the embolic beads used were 1,000 μm in diameter. The data show that, despite repeated embolic injury by polystyrene beads of different diameters, there was no significant increase in total V˙H. The acinar component of SnIII, which represents V˙H in the distal airways, accounts for over 90% of the totalV˙H. The conductive component of SnIII, which represents V˙H between larger conductive airways, remains relatively constant and a minor component. We conclude that pulmonary microembolism does not result in significant redistribution of ventilation.
Publisher
American Physiological Society
Subject
Physiology (medical),Physiology
Cited by
12 articles.
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