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J Appl Physiol 79: 929-940, 1995;
8750-7587/95 $5.00
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Journal of Applied Physiology, Vol 79, Issue 3 929-940, Copyright © 1995 by American Physiological Society

ARTICLES

Modeling steady-state inert gas exchange in the canine trachea

S. C. George, J. E. Souders, A. L. Babb and M. P. Hlastala
Department of Chemical Engineering, University of Washington, Seattle 98195-6540, USA.

The functional dependence between tracheal gas exchange and tracheal blood flow has been previously reported using six inert gases (sulfur hexafluoride, ethane, cyclopropane, halothane, ether, and acetone) in a unidirectionally ventilated (1 ml/s) canine trachea (J. E. Souders, S. C. George, N. L. Polissar, E. R. Swenson, and M. P. Hlastala. J. Appl. Physiol. 79: 918-928, 1995). To understand the relative contribution of perfusion-, diffusion- and ventilation-related resistances to airway gas exchange, a dynamic model of the bronchial circulation has been developed and added to the existing structure of a previously described model (S. C. George, A. L. Babb, and M. P. Hlastala. J. Appl. Physiol. 75: 2439-2449, 1993). The diffusing capacity of the trachea (in ml gas.s-1.atm-1) was used to optimize the fit of the model to the experimental data. The experimental diffusing capacities as predicted by the model in a 10-cm length of trachea are as follows: sulfur hexafluoride, 0.000055; ethane, 0.00070; cyclopropane, 0.0046; halothane, 0.029; ether, 0.10; and acetone, 1.0. The diffusing capacities are reduced relative to an estimated diffusing capacity. The ratio of experimental to estimated diffusing capacity ranges from 4 to 23%. The model predicts that over the ventilation-to-tracheal blood flow range (10-700) attained experimentally, tracheal gas exchange is limited primarily by perfusion- and diffusion-related resistances. However, the contribution of the ventilation-related resistance increases with increasing gas solubility and cannot be neglected in the case of acetone. The increased role of diffusion in tracheal gas exchange contrasts with perfusion-limited alveolar exchange and is due primarily to the increased thickness of the bronchial mucosa.


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