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HANDBOOK OF PHVSIOLC5GV 



NEUROPHYSIOLOGY II 



postsympathectomy reflex vasodilalor responses dis- 

 appeared. 



Nor has direct stimulation of tiie \asodilator region 

 in the medulla oblongata yielded evidence of the 

 existence of vasodilator nerves [Lindgren & Uvnas 

 (153, 154), Frumin et al. (93)]. A cross-circulation 

 technique permitting the blood flow to be studied 

 independently of the falls in arterial pressure revealed 

 very substantial rises of blood flow in muscles and 

 cutaneous vessels of the cross-perfused leg. Neither of 

 the above-named groups of authors were able to find 

 even the slightest increase of flow in muscles or skin 

 after sympathectomy. Sensory denervation (section of 

 the spinal cord below L4), on the other hand, had no 

 influence whatsoever on the vasodilator efTects that 

 were produced by stimulation of the depressor area. 



Bach (19) is one of the last advocates of the vaso- 

 dilator center theory. In his opinion the dorsal root 

 vasodilator system exerts a tonic vasodilator control. 

 Using cats in which almost the whole spinal cord was 

 exposed, he developed a method for rapid and com- 

 plete section of all the dorsal or ventral nerve roots 

 from the fourth cervical to the fourth lumbar nerves. 

 In those cats in which the arterial pressure at the 

 start of the experiment was sufficiently high (100 to 

 1 30 mg Hg) to permit a study of depressor reflexes, 

 stimulation of a depressor nerve produced a slow, 

 but well-defined, decrease in arterial pressure. Fol- 

 lowing resection of all the dorsal roots the pressure 

 rose 20 to 40 mm Hg, from which Bach concluded 

 that these nerves normally exerted a vasodilator tone. 

 The fact that no depressor reflexes were obtained in 

 the deafferented animal, even though the sympa- 

 thetic vasoconstrictor innervation was intact, provided 

 "direct evidence that the dorsal root fibers are an 

 essential pathway for initiation of the reflex vasodilata- 

 tion." 



Against Bach's conclusion the objection can be 

 raised that inhibition of vasoconstrictor tone has been 

 indisputably demonstrated in depressor reflexes. Ap- 

 parently in Bach's experiments the animals were in 

 such poor condition that vasoconstrictor tone had 

 disappeared. It may be added that cutting of the 

 dorsal roots with the technique used by Bach was 

 bound to evoke a violent discharge, with reflex vaso- 

 constriction and adrenal secretion, so raising the 

 arterial pressure. 



Since antidromic vasodilator impulses were con- 

 sidered chiefly to pass to the skin, they might con- 

 ceivably mediate cutaneous vasodilatation of central 

 origin. Folkow and his associates (88, 89) produced 



marked vasodilatation in the skin of the cat paw by 

 diathermic heating in the temperature-regulating 

 area of the anterior part of the hypothalamus. 

 Sympathectomy — acute or chronic — completely abol- 

 ished this response; however, it remained unchanged 

 after sensory denervation of the paw. 



On the basis of the accumulated experimental evi- 

 dence it is, therefore, safe to conclude that there 

 exists no centrally controlled antidromic vasodilator 

 outflow via dorsal root fibers. Such a statement does 

 not, of course, mean that antidromic vasodilator 

 nerves are nonexistent. On the contrary, antidromic 

 vasodilator impulses certainly play an important role 

 in the local regulation of cutaneous circulation. How- 

 ever, the physiology of axon reflexes is beyond the 

 scope of this article. 



As mentioned above, parasympathetic \asodilator 

 nerves were also thought to be involved in Bayliss' 

 vasomotor regulation mechanism. The experimental 

 evidence for the participation of these nerves in pressor 

 and depressor reflexes is even less impressive than for 

 that of dorsal root fibers. Celander & Folkow (52), 

 like Lindgren & Uvnas (153, 154), were unable to find 

 any evidence of an activation of parasympathetic 

 vasodilator fibers to the tongue or the intestines in 

 depressor reflexes elicited by stimulation of aff"erent 

 vagal fibers or by direct electrical stimulation within 

 the medullary depressor area. 



The hypothesis of a bulbar vasodilator center im- 

 plies the existence in the medulla oblongata of an in- 

 tegrating area which relays incoming impulses to \ari- 

 ous vasodilator nerves. If the hypothesis were true, it 

 should be possible to activate the center by eliciting 

 reflex vasodilation or lay direct local stimulation of 

 the structures in question. 



Since vasodilator nerve discharges occur neither in 

 depressor reflexes evoked by afferent stimulation of a 

 sinus, a vagus or a peripheral sensory nerxe, nor in 

 vasodilatation produced by stimulation in tiie de- 

 pressor area, the aforementioned requirements for 

 the existence of a vasodilator center within the de- 

 pressor area are lacking. On the whole, there seems 

 no reason whatsoever to assume the existence of a 

 bulbar vasodilator center in the sense' that this center 

 would form an integrative area governing the activity 

 in the various vasodilator nerve outflows. 



It is true that a discharge in the sympathetic saso- 

 dilator nerves to the skeletal muscles can be brought 

 about by direct stimulation within a 'vasodilator 

 band' running in the rostrocaudal direction in the 

 ventrolateral part of the medulla oblongata. How- 



