434 PHYSIOLOGY CHAP. 



classical form in which it has ever been recorded. At the first 

 moment of expiration the arterial pressure rises, falling in the 

 second period ; in the first period of inspiration it continues to 

 fall, and then rises at the second. Arterial pressure therefore 

 reaches its maximum in the first period of expiration, and its 

 minimum in the first period of inspiration. 



In explanation of this fact Einbrodt assumes that the 

 inspiratory fall of intrathoracic pressure, by determining an 

 acceleration of the venous current, favours the diastolic refilling of 

 the heart, which is followed by a larger systolic outflow, raising 

 arterial pressure. This increase is maximal during the first 

 period of expiration, either on account of the previous excess 

 filling of the heart, or from the expiratory increase of intrathoracic 

 pressure, which favours the centrifugal course in the arteries and 

 the systolic action of the heart. In the second period of expira- 

 tion the arterial pressure falls owing to retardation of the venous 

 current in the blood, which diminishes the diastolic refilling and 

 systolic emptying of the heart. 



This theory is inadequate, because it takes no account of 

 the pressor influence of the abdominal muscles, which is capable 

 of raising arterial pressure during expiration, by compressing 

 the capillaries of the vessels belonging to the intra-abdominal 

 aortic system. 



Funcke and Latschemberger (1877) held the fundamental 

 cause of the phenomenon to lie in the changes of capacity in the 

 capillary pulmonary system, effected by the alternate dilatation 

 and retraction of the lungs, the respiratory oscillations of pressure 

 in the thoracic cavity being only of secondary importance. They 

 found in fact that in curarised rabbits, during artificial respirations 

 by the bellows, with open thorax, there were still respiratory 

 oscillations of carotid pressure. They explained this fact by 

 admitting that when the alveoli of the lung dilate (whether from 

 positive tracheal, or from negative pleural pressure) the capillary 

 network which they contain must become stretched, with a 

 consequent elongation and constriction of the vascular lumen, 

 resulting in a considerable diminution in their capacity. The 

 opposite changes must occur at each expiratory retraction of the 

 pulmonary alveoli, which increases the capacity of the capillary rete. 

 Given these effects of the respiratory movements, they must not 

 merely influence the course of the blood in the lesser circulation, 

 but must also act indirectly upon the pressure of the aortic 

 system, which is fed from the pulmonary blood. The inspiratory 

 increase in pressure would depend upon the expulsion of the 

 blood from the compressed pulmonary capillary system into the 

 left heart ; the expiratory fall of pressure, on the retention of the 

 blood in the newly dilated capillaries of the lungs. 



This theory, if not wholly unfounded, is at any rate very 



