956 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



intravascular volume rather than an increase in 

 extravascular volume (106) has been shown by 

 Mehrizi and Hamilton (79) using calculations from 

 mean transit time. It has been attributed classically to 

 constriction of efferent glomerular arterioles and a 

 passive distention of upstream vessels. 



In short, changes in vascular volume as a result of 

 increased resistance to flow can be attributed to any 

 combination of three causes, all operating at the same 

 time: /) decreased volume of constricting vessels, 2) 

 decreased distention of downstream vessels, and 5) 

 increased distention of vessels upstream to the site of 

 preponderant increase in resistance. The net change 

 in vascular volume will, then, depend on the location 



fig. 26. Hypothetical plots of the pressure drops in various 

 portions of the terminal vascular bed during a control state, 

 solid line; during a state of increased precapillary resistance, 

 dash-dot line; and increased postcapillary resistance, dashed line. 



of the resistance increase in the morphological pattern 

 of the vascular network. A lessening of resistance in 

 any part of the network will presumably induce oppo- 

 site changes in vascular volume. These structures are 

 affected differentially by various vasoactive agents. 

 Data are insufficient at present to draw significant 

 generalizations regarding the various vascular beds. 



PULSATILE CHANGES IN VASCULAR VOLUME 



Pulsatile flow through a dog's ulnar artery was 

 measured with a square wave electromagnetic flow- 

 meter together with pressure recorded in a small 

 branch just proximal to the flowmeter and with paw 

 volume pulse recorded plethysmographically (fig. 27). 

 The flow record showed a dicrotic notch but never 

 fell to or below zero during diastole. A volume pulse 

 calculated by integrating the flow pulse and sub- 

 tracting an assumed constant venous output was 

 essentially similar (fig. 27). Both showed two humps 

 of approximately similar magnitude. 



In man, the normal digital volume pulse rises 

 relatively more rapidly than that of the dog's paw, 

 has a sharp peak at the end of the first quarter of the 

 pulse interval, and a slight notch about halfway down 

 the descending limb (fig. 28). If the supplying artery 

 is occluded but adequate collateral circulation is 

 available, the digital pulse shows a peak which is 

 rounded and delayed, and the notch on the descending 

 limb is absent. In the presence of vasospastic disease, 

 the peak may be delayed slightly, the notch raised or 

 may occur sooner on the descending limb, and the 

 area of pulse per unit amplitude increased in com- 

 parison with the normal. With elevation of venous 

 pressure or interference with venous outflow, the peak 

 of the pulse is sharper than normal and a second hump 



Pulsatile arterial inflow Pulsatile orteriol pressure Pulsatile plethysmogroph vol Calculated pulsatile vol 



fig. 27. Records of A — pulsatile arterial inflow; B — pulsatile arterial pressure; and C — pulsatile 

 plethysmographic volume, in the dog's paw. Arterial inflow recorded with an electromagnetic meter 

 on the ulnar artery. D — pulsatile volume calculated from the pulsatile arterial inflow, assuming a 

 constant venous outflow. 



