74 



Scientific Proceedings (72). 



asthma and emphysema, we noted (1) low pulse pressure in those 

 cases uncomplicated by atherosclerosis, probably due to a dim- 

 inished systolic volume; (2) the loud pulmonic second sound 

 pointing towards increased resistance in the lesser circulation; 

 (3) polycythemia, possibly a teleologic phenomenon designed to 

 compensate for a lessened minute volume output from the left 

 ventricle; (4) enlarged veins in the neck and cyanosis suggesting 

 a certain amount of venous stasis. These observations led us to 

 believe that there was considerable circulatory disturbance in 

 conditions associated with obstructed expiration. 



Due to the lack of adequate clinical material, we decided to 

 study this subject in the experimental animal. 



Dogs were used. A saturated solution of chloretone and mor- 

 phine was employed for inducing anesthesia. A T-tube was in- 

 serted into the trachea. (There was no increase in the dead space.) 

 The C0 2 in the blood was determined by the method of Barcroft 

 and Haldane; that in the alveolar air according to Henderson's 

 method. (Inspiratory samples were taken.) The minute volume 

 was determined by means of a Dreser tube for collecting expired 

 air. We first did a series of controls and found that the C0 2 

 content of the blood and of the alveolar air varied with the minute 

 volume, thus corroborating the work of Haldane and Priestley. 

 Anesthesia produced effects varying only with the ventilation. 

 In another series we inserted a valve which worked only one way 

 and produced obstruction to expiration for varying lengths of 

 time. This was our method of simulating the asthmatic attack. 

 Control determinations were made before the use of the valve was 

 begun. We found a marked increase in the C0 2 content of both 

 the blood and the alveolar air, especially where compensation had 

 not occurred. In most cases there was an attempt at compensa- 

 tion with regard to increased ventilation, due to the sensitiveness 

 of the respiratory center to slight rises in the CO2 pressure in the 

 alveolar air. As soon as the obstruction was introduced, the type 

 of breathing changed, expiration became long drawn out, the rate 

 slowed, the abdominal wall muscles also taking part in the attempt 

 to force air out. We thought therefore that increased muscular 

 work might be a factor tending to raise the CO2 content of the 

 blood. 



