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Journal of Applied Physiology, Vol 51, Issue 1 26-32, Copyright © 1981 by American Physiological Society
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P. L. Klineberg, K. Rehder and R. E. Hyatt
Lung volumes, static pressure-volume curves, maximal expiratory flow-volume curves, right-to-left intrapulmonary shunts (Qs/Qt), and distributions of ventilation and perfusion relative to the alveolar ventilation and perfusion ration (VA/Q) were determined in seated normal men before chest strapping while breathing air (Cair) and during chest strapping while breathing air (Sair) or 100% oxygen (So2). With Sair and So2, mean vital capacity was reduced by 44% from control. Elastic recoil pressure [Pst(L)] of the lung at 50% control total lung capacity (TLC) increased significantly (P less than 0.05) from 4.64 +/- 0.39 cmH2O (mean +/- SE) to 7.00 +/- 0.47 cmH2O with Sair and to 7.24 +/- 0.70 cmH2O with So2. Maximal expiratory flow at 50% of control TLC increased significantly (P less than 0.05) from 3.22 to 0.25 l/s (mean +/- SE) to 5.84 +/- 0.69 l/s with Sair and to 5.50 +/- 0.68 l/s with So2. With Sair, no significant increase in Qs/Qt from control was observed. With So2, mean Qs/Qt increased significantly (P less than 0.05) from 0 to 2.2 +/- 0.9% of the cardiac output. It is therefore unlikely that the development of atelectasis, as indicated by an increase in Qs/Qt, accounts for the increase in Pst (L) with Sair and So2. Current evidence suggests that either change in alveolar surface compliance or distortion of the lung or both are responsible for the increased recoil pressure but that neither mechanism alone appears to explain it totally.
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