CIRCULATION IN SKELETAL MUSCLE 



'375 



found that temporary occlusion of the circulation 

 through the cat's hind limb (paw tied off) was 

 followed by reactive hyperemia. As the condition 

 of the animal deteriorated, basal tone diminished and 

 reactivity of the vessels decreased. Reactive hyperemia 

 in skeletal muscles is soon lost when they are per- 

 fused with saline. 



It is generally agreed that reactive hyperemia 

 takes place independently of nervous connections. 

 Bayliss (35) thought that the relaxation of the vessels 

 during reactive hyperemia was due to lengthening of 

 the plain muscle because, during the period of ar- 

 rested circulation, the fibers were no longer subjected 

 to the stimulus of stretch. Lewis ( 1 38) denied this 

 because reactive hyperemia followed circulatory 

 arrest by venous occlusion, during which the smooth 

 muscle of the arterial walls was still distended by 

 the arterial blood pressure. He did numerous ex- 

 periments leading him to the conclusion that the 

 response was due to the action of a histamine-like 

 vasodilator substance the concentration of which, 

 in the tissue fluids, increased during the ischemic 

 period. Folkow et al. (95) and Emmelin & Emmelin 

 (80) found that reactive hyperemia occurred quite 

 normally in the limbs of animals in which the action 

 of injected histamine had been completely blocked by 

 antihistaminics. Therefore, they concluded that the 

 response was probably not due to the action of a 

 histamine-like substance. Guyton et al. (62) showed 

 that reactive hyperemia cannot be due to the action 

 of accumulated CO 2. Ventilating dogs with 20 per 

 cent CO 2 was not accompanied by any vasodilatation 

 in the legs. On the other hand, reduction of the 

 oxygen saturation of the blood to 30 per cent doubled 

 the rate of the blood flow. Guyton et al. thought that 

 oxygen deficiency might well be one of the causes of 

 reactive hyperemia. 



Most studies of reactive hyperemia in muscle in 

 man have been made in the forearm or calf using 

 venous occlusion plethysmography. However, one 

 must alwavs remember that the blood flows recorded 

 by this method are not those in the skeletal muscle 

 only, but include also the blood flow through the 

 skin. 



In man as in animals (120), the longer the period 

 of arrest lasts the greater is the subsequent hyperemia 

 in the forearm ( 1 58) ; the increase is mainly in the 

 duration of high flows, the peak value being relatively 

 little increased. Reduction of the arterial pressure 

 during the period of arrest and of the stimulus of 

 stretch may be partlv responsible for the loss of 

 vascular tone (156). Exposing the forearm to sub- 



atmospheric pressure and thus '"packing" it with 

 blood before arresting the circulation lessens the fall 

 of intravascular pressure during the period of oc- 

 clusion. As in animals, so in the human forearm, 

 antihistamines, such as tripelennamine, mepyramine, 

 and antazoline when introduced into the brachial 

 artery do not diminish the reactive hyperemia that 

 follows 3 min of circulatory arrest, although they 

 completely abolish the increase in flow brought 

 about by the intra-arterial injection of histamine 



(70- 



Apart from histamine, various chemical causes, 

 such as anoxia, have been suggested to explain reac- 

 tivity in man. Lewis (138) says, "'It is manifest that 

 neither deficiency of oxygen nor an accumulation 

 of carbon dioxide or other weak acid in the blood 

 that is within the vessels can possibly form the direct 

 stimulus; were that so the reaction would always be 

 fleeting, the blood being at once replaced by the flood 

 of the reactive hyperaemia." Certainly the vessels 

 would be filled with fresh blood almost instantly, but 

 does it follow that the reaction would be fleeting? 

 After sudden removal of the stimulus how fast in 

 fact would the vessels contract? Some kinds of plain 

 muscle respond to stimulation rather slowly. Further 

 experiments are needed on this important point. 

 McNeill (148) showed that during the second minute 

 of a reactive hyperemia in the forearm the oxygen 

 saturation of the venous blood in the antecubital 

 vein may rise transiently to well above the resting 

 value. The effect is seen in figure 21. The reason for 

 this transient rise in venous oxygen saturation, as 

 McNeill showed, was that oxygen consumption re- 

 turned to the resting level more promptly than did 

 the blood flow; this corresponded to a transient de- 

 crease in utilization. Return of the blood flow to the 

 pre-occlusion level may have lagged behind restora- 

 tion of the circulation a) because of the presence of a 

 nonoxidizable metabolite, or b) because the vessels 

 simply could not contract fast enought to keep pace 

 with the rapid fall of the concentration of some 

 oxidizable vasodilator metabolite. Further work is 

 necessary on this topic. 



Dornhorst & Whelan (68) showed that, after a 

 short period of arrest of the circulation in the calf, 

 the rate at which the blood flow during the subse- 

 quent reactive hyperemia returns to initial levels is 

 exponential; i.e., a straight line is obtained when log 

 flow is plotted against time (compare fig. 24Z?). The 

 significance of this fact is not clear. In other experi- 

 ments, using a pressure plethysmograph, they studied 

 the effect on reactive hyperemia of reduction of the 



