CENTRAL CARDIOVASCULAR CONTROL 



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the muscle blood flow e\-en if the orsjanism is not 

 under stress. It is well known that the initiation of 

 voluntary muscular actis'ity is accompanied by in- 

 stantaneous, or even anticipatory adjustments in the 

 respiratory and circulatory systems to meet the in- 

 creased metabolic demands, adjustments occurring 

 with such rapidity that the effector mechanisms are 

 necessarily nervous. .Since the vasodilator neurons 

 have their origin in the motor cortex, they may be 

 concerned in some way with the initial adjustment of 

 the muscle blood flow during exercise. 



Although the sympathetic va.sodilator ner\es may 

 pla\' .some part in the initial rise of blood flow in the 

 muscles at the start of muscular exercise, they are not 

 necessarily involved in the regulation of the muscle 

 blood flow during e.xercise. Numerous British inves- 

 tigators have shown, in both animals and man, that 

 adequate vasodilatation occurs during e.xercise even 

 in the muscles of a sympathectomized extremity. 



No evidence has emerged to show that the sympa- 

 thetic vasodilator nerves are involved in depressor 

 reflexes, at least in anesthetized animals. The de- 

 pressor center of the medulla oblongata can be de- 

 stroyed locally, and medullary vasodepressor reflexes 

 thus abolished, without affecting the sympathetic 

 vasodilator pathway. 



The sympathetic vasodilator tract, and also those 

 vasoconstrictor fibers that accompany it, does not 

 appear to exert any tonic influence on skeletal 

 muscle vessels, again in anesthetized animals, since 

 in them section of the pathways in their medullary 

 portion does not affect the blood flow in the skeletal 

 muscles. 



OBSOLETE VASODILATOR CENTER HYPOTHESIS 



When Bayliss early this century propounded his 

 vasodilator center theory, which he subsequently 

 elaborated in his monograph of 1923 (29), he as- 

 sumed that this center had not only an inhibitory re- 

 ciprocal action on the vasoconstrictor center, but also 

 exerted a direct influence on the tone of the peripheral 

 vascular bed by tonic discharges via vasodilator 

 nerves. In his view, gained from experiments on dogs 

 and rabbits, the sympathetic vasoconstrictor tone 

 was slight or quite inappreciable in those animals. He 

 was therefore obliged to attribute depressor reflexes 

 largely to excitation of vasodilator nerves rather than 

 to inhibition of vasoconstrictor tone. Since Bayliss 

 was unaware of the existence of sympathetic vaso- 

 dilator nerves, he had to seek vasodilator nerves of 



nonsympathetic origin. It was reasonaiile for him to 

 assume that these should be sought in the dorsal root 

 fibers since both his own observations and those of 

 Strieker (196) had shown that mechanical and elec- 

 trical stimulation of those fibers could produce anti- 

 dromic vasodilatation. Moreov^er, parasyinpathetic 

 vasodilator fibers were known, and they were assumed 

 to take part in the central \asodilator nerve control 

 of the peripheral \ascular bed. 



With our present knowledge of the physiology of 

 the central ner\ous system, it is scarcely plausible 

 that vasodilator impulses would be directed from the 

 medulla oblongata in an antidromic direction, via 

 afferent fibers, to the skin and mu.scles. It was to 

 these areas that the antidromic vasodilator impulses 

 were considered to lead. All experimental experience 

 indicates that such a reversed synapse passage is un- 

 likely under physiologic conditions. It is also diffi- 

 cult to conceive of two flows of impulses in opposite 

 directions passing through one and the same neuron 

 without entering areas refractory to each other and 

 hence being abolished. It is astonishing to find that 

 this notion of the centrally controlled antidromic 

 vasodilator outflow still persists today, in spite of its 

 inherent implausibilities. 



Bayliss' experimental evidence, as discussed in 

 detail by Uvnas (204) and Folkow el al. (89), is by no 

 means unimpeachable. One of his chief arguments 

 was that depressor nerve stimulation produced reflex 

 vasodilatation in an extremity even after sympathec- 

 tomy. Yet he observed that vasodilator responses 

 were not always abolished by complete denerv-atioii of 

 the leg. This finding should have aroused his suspi- 

 cions, but rather surprisingly he stated that "these ex- 

 periments were naturally rejected." Dole & Morison 

 (65) conducted experiments on dogs and cats with a 

 plethysmographic technique largely conforming to 

 that of Bayliss and found that a depressor reflex was 

 sometimes attended by an increase in the leg volume, 

 not only after sympathectomy, but even after total 

 denervation of the leg — i.e. even after section of the 

 afferent innervation — and they therefore concluded 

 that the vasodilatation could not be of nervous origin. 



Frumin et al. {93) employed a cross-circulation 

 technique, measuring the blood flow in the femoral 

 artery. With depressor reactions elicited in different 

 ways, they obser\ed an increase of blood flow in the 

 cross-perfused leg. This reflex increase generally dis- 

 appeared after .sympathectomy, but whenever it per- 

 sisted it was due to the presence of an overlooked 

 collateral circulation in the cross-perfused leg. The 

 moment this collateral circulation was eliminated, all 



