MODELING STEADY-STATE INERT-GAS EXCHANGE IN THE CANINE TRACHEA

The functional dependence between tracheal gas exchange and tracheal b lood flow has been previously reported using six inert gases (sulfur h exafluoride, 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. App l. Physiol. 79: 918-928, 1995). To understand the relative contributio n of perfusion-, diffusion- and ventilation-related resistances to air way gas exchange, a dynamic model of the bronchial circulation has bee n developed and added to the existing structure of a previously descri bed model (S. C. George, A. L. Babb, and M. P. Hlastala. J. Appl. Phys iol. 75: 2439-2449, 1993). The diffusing capacity of the trachea (in m l gas . s(-1) . atm(-1)) was used to optimize the fit of the model to the experimental data. The experimental diffusing capacities as predic ted by the model in a 10-cm length of trachea are as follows: sulfur h exafluoride, 0.000055; ethane, 0.00070; cyclopropane, 0.0046; halothan e, 0.029; ether, 0.10; and acetone, 1.0. The diffusing capacities are reduced relative to an estimated diffusing capacity. The ratio of expe rimental to estimated diffusing capacity ranges from 4 to 23%. The mod el predicts that over the ventilation-to-tracheal blood flow range (10 -700) attained experimentally, tracheal gas exchange is limited primar ily by perfusion- and diffusion-related resistances. However, the cont ribution of the ventilation-related resistance increases with increasi ng gas solubility and cannot be neglected in the case of acetone. The increased role of diffusion in tracheal gas exchange contrasts with pe rfusion-limited alveolar exchange and is due primarily to the increase d thickness of the bronchial mucosa.