CH. XXVII.] EFFECT OF KESPIRATION ON CIKGULATION 38? 



increased supply of blood is then passed via the pulmonary circuit to 

 the left heart ; this takes a little time ; hence it is that the effect oi' 

 inspiration in raising arterial pressure is not seen at the very com- 

 mencement of the inspiration. In fact, in some animals which 

 normally breathe very quickly (for instance, the rabbit), inspiration 

 is over, and the next expiration has begun before the rise of blood- 

 pressure occurs. By making a rabbit breathe slowly (Fredericq 

 accomplished this by cooling the medulla oblongata), the tracing 

 obtained is similar to that which is got from an animal like a dog, 

 which normally breathes slowly. 



The delay which occurs in the inspiratory rise of arterial blood-pressure has 

 been attributed by some to an increase of the capacity of the pulmonary capillaries 

 brought about by the distension of the chest ; this sudden increase in the bed of 

 the stream would temporarily retard the rate of flow through the pulmonary 

 circuit. Recent research has, however, shown that even considerable changes in 

 the capacity of the blood-vessels of the lung, as, for instance, by shutting off the 

 entire circulation of one lung (Tigerstedt), have little or no influence on the 

 systemic pressure ; it is therefore extremely doubtful whether small changes such 

 as would be produced in ordinary breathing can have any effect on the inflow into 

 the left auricle. 



When the chest of an animal is freely opened, and artificial 

 respiration performed in order to keep it alive, respiratory undulations 

 on the arterial pressure-curve are still seen, but they are in the 

 reverse direction. These obviously cannot be produced in the 

 mechanical way just described. The forcible inflation with air at 

 first squeezes more blood out of the alveolar capillaries, that is, the 

 capacity of these vessels is diminished, and this theoretically might 

 increase the quantity of blood thrown into the left ventricle, and so 

 cause a rise of arterial pressure. But the main effect of increased 

 mtra-alveolar pressure is to produce an increased resistance to the pul- 

 monary circulation, and the rate of flow into the left side consequently 

 falls ; the aortic pressure therefore falls, while the pressure in the pul- 

 monary artery rises. If the high positive intrapulmonary air- 

 pressure persisted, a condition would soon be reached, in which the 

 increased blood-pressure in the pulmonary artery would lead to a 

 greater flow, and the aortic blood-pressure would remain constant ; this, 

 however, has been shown to take a much longer time than an ordinary 

 respiration period. Hence the effect of inflations of the lungs at the 

 ordinary respiration rate is to diminish the aortic blood-pressure; 

 this rises again, for the opposite reasons, in the intervals of deflation 

 which correspond to expiration. 



If artificial respiration is performed while the thorax is not opened, 

 a further complication arises from the fact that the increased intra- 

 pleural pressure decreases the rate of flow of blood into the thorax, 

 and under these conditions the blood-pressure in the pulmonary 

 artery falls, and in consequence the fall in the aortic blood-pressure 



