Soluble gas exchange in the pulmonary airways of sheep

We studied the airway gas exchange properties of five inert gases with different blood solubilities in the lungs of anesthetized sheep. Animals were ventilated through a bifurcated endobronchial tube to allow independent ventilation and collection of exhaled gases from each lung. An aortic pouch at the origin of the bronchial artery was created to control perfusion and enable infusion of a solution of inert gases into the bronchial circulation. Occlusion of the left pulmonary artery prevented pulmonary perfusion of that lung so that gas exchange occurred predominantly via the bronchial circulation. Excretion from the bronchial circulation (defined as the partial pressure of gas in exhaled gas divided by the partial pressure of gas in bronchial arterial blood) increased with increasing gas solubility (ranging from a mean of 4.2 × 10−5 for SF6 to 4.8 × 10−2 for ether) and increasing bronchial blood flow. Excretion was inversely affected by molecular weight (MW), demonstrating a dependence on diffusion. Excretions of the higher MW gases, halothane (MW = 194) and SF6 (MW = 146), were depressed relative to excretion of the lower MW gases ethane, cyclopropane, and ether (MW = 30, 42, 74, respectively). All results were consistent with previous studies of gas exchange in the isolated in situ trachea.

Tracheal gas exchange: perfusion-related differences in inert gas elimination

Exchange of inert gases across the conducting airways has been demonstrated by using an isolated dog tracheal preparation and has been characterized by using a mathematical model (E. R. Swenson, H. T. Robertson, N. L. Polissar, M. E. Middaugh, and M. P. Hlastala, J. Appl. Physiol. 72: 1581–1588, 1992). Theory predicts that gas exchange is both diffusion and perfusion dependent, with gases with a higher blood-gas partition coefficient exchanging more efficiently. The present study evaluated the perfusion dependence of airway gas exchange in an in situ canine tracheal preparation. Eight dogs were studied under general anesthesia with the same isolated tracheal preparation. Tracheal perfusion (Q) was altered from control blood flow (Qo) by epinephrine or papaverine instilled into the trachea and was measured with fluorescent microspheres. Six inert gases of differing blood-gas partition coefficients were used to measure inert gas elimination. Gas exchange was quantified as excretion (E), equal to exhaled partial pressure divided by arterial partial pressure. Data were plotted as ln [E/(l-E)] vs. In (Q/Qo), and the slopes were determined by least squares. Excretion was a positive function of Q, and the magnitude of the response of each gas to changes in Q was similar and highly significant (P < or = 0.0002). These results confirm a substantial perfusion dependence of airway gas exchange.

Modeling steady-state inert gas exchange in the canine trachea

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.

Conducting airway gas exchange: diffusion-related differences in inert gas elimination

We studied CO2 and inert gas elimination in the isolated in situ trachea as a model of conducting airway gas exchange. Six inert gases with various solubilities and molecular weights (MW) were infused into the left atria of six pentobarbital-anesthetized dogs (group 1). The unidirectionally ventilated trachea behaved as a high ventilation-perfusion unit (ratio = 60) with no appreciable dead space. Excretion of higher-MW gases appeared to be depressed, suggesting a MW dependence to inert gas exchange. This was further explored in another six dogs (group 2) with three gases of nearly equal solubility but widely divergent MWs (acetylene, 26; Freon-22, 86.5; isoflurane, 184.5). Isoflurane and Freon-22 excretions were depressed 47 and 30%, respectively, relative to acetylene. In a theoretical model of airway gas exchange, neither a tissue nor a gas phase diffusion resistance predicted our results better than the standard equation for steady-state alveolar inert gas elimination. However, addition of a simple ln (MW) term reduced the remaining residual sum of squares by 40% in group 1 and by 83% in group 2. Despite this significant MW influence on tracheal gas exchange, we calculate that the quantitative gas exchange capacity of the conducting airways in total can account for less than or equal to 16% of any MW-dependent differences observed in pulmonary inert gas elimination.