THE CIRCULATION OF THE BLOOD 327 



be applied to the vascular system for determining the effects upon 

 arterial pressure of changes in the heart-beat. 



Modifications of Arterial Pressure by Changes in the Peripheral 

 Resistance. If while the pump c in Fig. Ill is steadily sending 

 a given volume of liquid per minute into B the resistance at D' 

 increase, it is clear arterial pressure must rise. For B is only 

 stretched enough to squeeze out in a minute the given quantity 

 of liquid against the original resistance, and cannot at first send 

 out that quantity against the greater. Liquid will consequently 

 accumulate in it until at last it becomes stretched enough to send 

 out as much in a minute as before in spite of the greater resistance 

 to be overcome. A new mean pressure at a higher level will then 

 be established. If, on the contrary, the resistance diminishes 

 while the pump's work remains the same, then B will at first 

 squeeze out in a minute more than it receives, until finally its 

 elastic pressure is reduced to the point at which its receipts and 

 losses balance, and a new and lower mean pressure will be estab- 

 lished in B. 



Similarly in the vascular system, increase of the peripheral 

 resistance by narrowing of the small arteries will increase arterial 

 pressure in all parts nearer the heart, while dilatation of the small 

 arteries will have the contrary effect. 



Summary. We find then that arterial pressure at any moment 

 is dependent upon: (1) the quantity of blood forced into the ar- 

 teries in a given time; (2) the caliber of the smaller vessels. Both 

 of these and consequently the capillary circulation which depends 

 upon arterial pressure, are under the control of the nervous sys- 

 tem (see Chaps. XX and XXII). 



The Pulse. When the left ventricle contracts it forces a cer- 

 tain amount of blood into the aorta, which is already distended 

 and on .account of the resistance in front cannot empty itself as 

 fast as the contracting ventricle fills it. As a consequence its 

 elastic walls yield still more it enlarges both transversely and 

 longitudinally and if exposed in a living animal can be seen and 

 felt to pulsate, swelling out at each systole of the heart, and 

 shrinking and getting rid of the excess during the pause. A 

 similar phenomenon can be observed in all the other large arteries, 

 for just as the contracting ventricle fills the aorta faster than the 

 latter empties (the whole period of diastole and systole being 



