CIRCULATION IN SKELETAL MUSCLE 



'363 



I - SYMPATHETIC CHAIN 

 DIVIDINO PLANE 



fig. 9. Preparation used for investi- 

 gating the effect of stimulation of the 

 baroreceptors on muscle blood flow. 

 [After Folkow et al. (101).] 



& Uvnas (ioq, 104) have shown that the transmitter 

 is probably noradrenaline. It is not adrenaline. Proof 

 of this was obtained in cats given Dibenamine. Other 

 procedures excluded the action of the vasodilator 

 fibers. After giving Dibenamine, stimulation of the 

 vasoconstrictors caused only weak contraction or 

 none at all. Injections of noradrenaline likewise 

 caused weak contraction or had no effect. On the 

 other hand, injections of adrenaline caused marked 

 vasodilatation in the muscle. From such results 

 Folkow and Uvnas concluded that the vasocon- 

 strictor nerve endings in the muscles of the cat (102) 

 and dog (104) might have released noradrenaline 

 but they had not released adrenaline. For a proper 

 account of these beautiful experiments and for the 

 literature, their papers should be consulted. Nor- 

 adrenaline has not yet been positively identified in 

 the venous effluent collected from a muscle vein 

 during vasoconstrictor nerve stimulation. 



EFFECT OF STIMULATION OF THE ARTERIAL BARO- 

 RECEPTORS ON SKELETAL MUSCLE VESSELS IN THE DOG. 



Folkow et al. (101) have shown that the sympathetic 

 vasoconstrictor fibers are solely responsible for medi- 

 ating the baroreceptor reflex. Their proof is as follows. 

 Figure 9 shows the preparation of the hind parts of 

 one dog (the recipient) which were perfused from 

 another dog (the donor); changes in blood pressure 

 and in hormone concentration in the upper part of 

 the recipient's body could not affect the circulation 



in its hind legs. The venous outflow from the hind 

 legs, mainly from the muscles, was recorded, as 

 was that from an area of the hind-leg skin. The re- 

 sults are seen in figure 10. Reduction of the blood 

 pressure in the recipient's carotid sinuses, by carotid 

 occlusion, caused vasoconstriction in both muscle 

 and skin. After section of the abdominal sympathetic 

 nerves neither carotid occlusion nor stimulation of 

 the carotid sinus .terve had any effect whatsoever. 

 Dorsal root fibers could not have been implicated. 

 They could have mediated vasodilatation, as acetyl- 

 choline injections did. And they were still in good 

 physiological condition because vasodilatation was 

 recorded in the skin when the dorsal roots were stimu- 

 lated (101). In other experiments the vasoconstrictor 

 action of the abdominal sympathetic chains was 

 blocked by Dibenamine. Clamping the carotids no 

 longer caused vasoconstriction in the legs. Although 

 the sympathetic vasodilator pathway remained in- 

 tact there was no sign of reciprocal innervation. On 

 the other hand, vasoconstriction in the legs following 

 carotid occlusion was normal after the dilator fibers 

 had been blocked by atropine (104). Folkow and his 

 colleagues concluded that the effect of stimulation of 

 the arterial baroreceptors on the blood flow in muscle 

 must be mediated solely by inhibition of activity in 

 the sympathetic vasoconstrictor fibers. 



EFFECT OF STIMULATION OF THE ARTERIAL BARORE- 

 CEPTORS ON THE CIRCULATION IN HUMAN SKELETAL 



