VENOUS RETURN 



1125 



and 160 cycles per min and in volume between o and 

 64 ml per cycle. In over 200 successive records not a 

 single instance of increased venous return occurred. 

 On the contrary, even the minutest increase in right 

 atrial pulsation always reduced venous return, and 

 very intensive pulsations actually reduced venous 

 return (at any given mean right atrial pressure) to as 

 low as 50 per cent of normal. Thus, there is a "rectifi- 

 cation phenomenon" occurring in the venous return 

 to the heart. That is, on the negative pressure cycle 

 collapse of the veins prevents very much enhance- 

 ment of venous return, while on the positive pressure 

 cycle, no such event prevents the positive pressure 

 from reducing venous return (29, 36, 37, 44, 113, 118, 

 141, 151). The net effect, based on both theoretical 

 grounds and experimental grounds, and supported 

 by studies from other laboratories as well as from our 

 own (54), is that central pulsations are not of any 

 value in promoting venous return. 



EFFECT OF LOCAL TISSUE ACTIVITY ON VENOUS RETURN — 

 EFFECT OF OXYGEN USAGE BY THE TISSUES. The best 



known condition in which local tissue activity affects 

 venous return is muscular exercise, in which case the 

 venous return may be increased several fold. Earlier 

 it was pointed out that this is caused both by an in- 

 crease in mean circulatory pressure and by vascular 

 dilatation in the muscles. The problem still remains, 

 however, to explain the cause of the vascular dilata- 

 tion in the muscles which in turn leads to the greatly- 

 enhanced venous return. In recent years, much evi- 

 dence has accumulated that oxygen usage by the 

 tissues might well be the initiating factor that con- 

 trols vascular dilatation (9, 41, 45, 51, 64, 65, 77, 79, 

 119, 125, 136, 190, 199). Some research workers have 

 felt that relative oxygen lack in the tissues causes them 

 to form a humoral substance which then causes vaso- 

 dilatation (7, 8, 15, 153). Humoral substances that 

 have been suspected are carbon dioxide, hydrogen 

 ions, adenosine phosphate compounds, histamine, 

 and lactic acid. Thus far, however, none of these 

 substances has been isolated in sufficiently large quan- 

 tities from the blood to prove that it is truly acting 

 as a vasodilator substance. 



Another concept is that the tissue cells compete 

 for the available oxygen in the arterial blood with 

 the vascular smooth muscle, perhaps with the smooth 

 muscle of the metarterioles and precapillary sphinc- 

 ters (45). If the tissues utilize excess oxygen, then 

 the blood vessels will be without adequate oxygen. 

 As a result, these vessels might dilate simply because 

 their smooth muscle walls cannot remain contracted 



in the face of oxygen lack. This concept is supported 

 by the following experiment : venous blood was re- 

 moved from the right ventricle, and arterial blood 

 was removed from the aorta of the same dog at the 

 same time. These two bloods were then alternately 

 passed through an isolated hind limb of a dog in which 

 the input and outflow pressures were controlled and 

 in which the blood temperature was very exactly 

 controlled. The arterial blood always caused vaso- 

 constriction, while the venous blood always caused 

 vasodilatation (to 250% of the arterial value). Fur- 

 thermore, the degree of vasodilatation depended al- 

 most proportionately on the degree of unsaturation 

 of the blood entering the limb as shown in figure 30. 

 The onlv difference between the two bloods was that 

 one had passed through the lungs and the other had 

 not. Therefore, if any vasodilator substance were in 

 the venous blood, then it would have to have been 

 removed by the lungs. Since the lungs are not known 

 to have this ability to remove vasodilator substances 

 of any type, and since controlled breathing of carbon 

 dioxide illustrated that carbon dioxide had no sig- 

 nificant local effect on peripheral vascular flow, we 

 must presume that it is lack of oxygen that initiates 

 the vasodilatation in the limb and not some inter- 

 mediary vasodilator substance. 



The reason for discussing this oxygen lack theory 

 of peripheral vasodilatation so completely is that, in 

 the final analvsis, it may be oxygen usage by the tis- 



100 



BLOOD FLOW (Per cent of control volue) 



100 



120 



WO 



160 



180 



200 



220 



240 



fig. 30. Effect of reducing arterial oxygen saturation on 

 the blood flow through an isolated hind limb of the dog. 

 [From Crawford el al. (45).] 



