Abstract
The theory has been advanced that changes in intrapleural pressure following alterations in bronchial caliber are mediated by carbon dioxide. 1 Thus in broncho-constriction, a gradual increase in carbon dioxide tension in the alveoli and blood seems to stimulate the inspiratory mechanism so that a relatively increased average thoracic girth results, and intrapleural pressure becomes more negative. If, however, stimulation of the respiratory center, by the direct administration of relatively high concentrations of carbon dioxide, becomes great enough to initiate active expiratory effort, then the intrapleural pressure becomes more positive than usual during expiration. 2 Since oxygen want in itself is, as was shown by Gasser and Loevenhart, 3 initially stimulating to the respiratory center, we thought it might be interesting to determine directly whether or not anoxemia would alter intrapleural pressure in the same way as increased carbon dioxide tensions.
Anoxemia was produced by rebreathing into a spirometer through a tracheal cannula. Carbon dioxide was absorbed by soda lime placed in the circuit. Gas analyses were made by means of a Hen-derson-Haldane-Bailey 4 apparatus in order to determine the degree of anoxemia produced and also to determine whether or not carbon dioxide was adequately absorbed. Blood gas analyses were also made in certain experiments. Details of our technique for estimating intrapleural pressure have been previously described. 5
Anoxemia produced by this method (18 experiments) was found uniformly to result in an initial gradual decrease in intrapleural pressure accompanied by an increased frequency and amplitude of respiration, and by a mean increase in thoracic girth. This primary effect corresponds to Loevenhart's initial stimulating action of oxygen want on the respiratory center, and seems to be exerted chiefly on the inspiratory mechanism.
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