Abstract
In our studies on the effects of broncho-constricting drugs on intrapleural pressure, 1 we noted that whereas a more positive intrapleural pressure on expiration developed following the administration of such drugs, it was by no means as great proportionally as the development of a more negative intrapleural pressure on inspiration. This suggested that mere broncho-constriction was not the only factor operating to produce the effects. Since resistance to the passage of air in and out of alveoli may be expected to increase gradually the CO2 tension in the alveoli, and in the blood, we determined to study directly the effects of CO2 inhalation on intrapleural pressure.
Dogs were lightly anesthetized with sodium amytal or with dial and urethane. The experimental technique employed has been previously described. 2 Inhalations of CO2 concentrations of 10% in oxygen (22 experiments) are followed by a gradual development of more negative intrapleural pressure than exists normally. The effect is similar to, but more marked and rapid than that noted after the administration of such broncho-constricting drugs as pilocarpine or eserine. It is accompanied by an increase in mean thoracic girth. Respiration, in other words, proceeds with the chest in an inspiratory position. This is probably due to the initial stimulating effect of CO2 en what Lumsden 3 postulated as the apneustic or inspiratory center in the medulla, and it probably is the cause of the more negative intrapleural pressure. Inhalations of concentrations of CO2 higher than 10% in oxygen (16 experiments) lead to a quick change in intrapleural pressure, in which it not only becomes much more negative on inspiration but also much more positive on expiration.
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