PERIPHERAL VENOUS SYSTEM 



io 95 



tor. This cold venoconstriction has a significant 

 reflex basis as well as a local component (18). As a 

 consequence, capillary pressure should rise, account- 

 ing for the increased transudation of fluid and the 

 tendency for the hematocrit to rise in cold. Second- 

 arily, the fall in temperature so interferes with dissocia- 

 tion of oxyhemoglobin as to produce some tissue 

 anoxia. The anoxic metabolites tend to act as vaso- 

 dilators competing with the cold constriction of the 

 arterioles, but seem to have no capacity to cause 

 venodilation. As a consequence, the skin becomes 

 plethoric because of some arterial inflow in the face 

 of a continued resistance to venous outflow. Rewarm- 

 ing of the tissue will now cause arteriolar dilation. 

 There is considerable evidence, however, that the 

 veins do not dilate in response to heat (39, 42, 56, 

 93). Indeed, the extreme venoconstriction produced 

 by the previous cold stimulus seems to dissipate 

 slowly after the tissue is rewarmed, so that during 

 the initial phase there is significant arteriolar dilation 

 in spite of persisting venous constriction (42). This 

 accounts for the extreme degree of plethora and 

 tendency toward edema formation which is observed 

 in the rewarming phase. 



Finally, attention should be called to fragmentary 

 information relating to the possibility of venovenous 

 reflexes. Apart from the general homeostatic regula- 

 tors of the circulation, such as the arterial presso- 

 receptor mechanism and the chemoreceptor responses, 

 are there mechanisms for adjusting venous capacity 

 as a function of the venous pressure? In view of the 

 importance of the central venous pressure in deter- 

 mining cardiac output, circulatory homeostasis 

 would be enhanced if there were such a mechanism 

 for adjusting venous capacity to central venous 

 pressure, so that the venous reservoir tended to 

 expand in response to an increase in venous pressure 

 and contract in response to a decrease in venous 

 pressure. 



There are several suggestions that such a mecha- 

 nism exists. With acute hypotension produced by 

 vagal bradycardia, Fleisch (26) observed an initial 

 venous constriction, attributable to the carotid 

 sinus reflex, followed by a secondary venous dilation 

 which he felt was associated with the venous conges- 

 tion produced by the bradycardia. A very similar 

 observation was reported by Schretzenmayr (82) in 

 the response to adrenergic drugs. Although these 

 drugs usually produced a conspicuous venocon- 

 striction, in instances where the circulatory load 

 became so great as to momentarily embarrass the 

 heart and produce cardiac distension, there appeared 



to be some mechanism that was counteracting the 

 venous constriction. More direct evidence of this 

 mechanism has been provided by the author (6), 

 who demonstrated venodilation to be produced 

 reflexly when venous congestion was produced by 

 inflating a balloon in the thoracic vena cava. It is 

 important to note, however, that to demonstrate 

 this effect it proved quite essential to prevent changes 

 in pressure on the arterial side of the circulation. 

 Unless such precautions are taken, the arterial 

 pressoreceptor system dominates the circulatory 

 responses, and the venovenous reflex mechanism 

 described above is completely overwhelmed. 



This dominance of the arterial pressoreceptor 

 reflexes accounts for a number of observations which 

 otherwise would argue against the venovenous 

 reflex. Wood (93) has demonstrated reflex venous 

 constriction in man associated with venous con- 

 gestion produced by occluding cuffs on the extremi- 

 ties. Inasmuch as they observed a reflex tachycardia 

 as well as arterial constriction associated with what 

 was estimated to be a 15 per cent reduction in cir- 

 culating blood volume, this response would relate 

 primarily to arterial pressoreceptor mechanisms. 

 In confirmation of this, when the subjects were in a 

 supine position so as to minimize pooling of blood 

 with venous tourniquets, neither the venous reflex 

 nor other signs of compensation to arterial hypoten- 

 sion were observed. Similarly, Page and co-workers 

 (68) found venoconstriction to be produced by the 

 Valsalva maneuver, which would also be explainable 

 in terms of baroreceptors on the arterial side dominat- 

 ing the simultaneous effects of congestion on the 

 venous side. 



There remains the problem of interpreting the 

 evidence presented by Burch (13) that patients in 

 congestive heart failure are characterized by an 

 augmented venomotor tone. If one assumes that the 

 only significant feature in this condition is venous 

 distention, this finding would not be compatible 

 with the postulation of a reflex venodilation in 

 response to venous distension. It may be of signifi- 

 cance that Burch found definite evidence of veno- 

 constriction only in those patients who were rather 

 severely decompensated and in whom numerous 

 other sources of reflex stimulation might therefore 

 have been operable. Our inability to define more 

 clearly the exact nature of the venomotor reactions 

 occurring in such an important clinical problem 

 should afford adequate stimulus to seek still further 

 clarification of the nature of venomotor control. 



