1 146 



HANDBOOK OF PHYSIOLOGY 



NEUROPHYSIOLOGY 11 



pressure or peripheral blood flow — are consistent in 

 showing that medullary vasomotor reflexes are effected 

 through variations in vasoconstrictor tone. \'asodila- 

 tation coincides with a decreased vasoconstrictor dis- 

 charge; vasoconstriction, with an increased dis- 

 charge. The question whether vasodilator nerves also 

 take part in medullary vasomotor reflexes has been 

 extensively discussed in past years. Until the 1930's it 

 was generally assumed, in accordance with Bayliss' 

 (29) view, that the medulla oblongata had two vaso- 

 motor centers, a vasoconstrictor and a vasodilator 

 center. These two centers had an inhibitory effect on 

 each other. Vasodilator impulses were thought to 

 pass from the vasodilator center (see p. 1155), partly 

 via parasympathetic \'asodilator fibers and partly via 

 dorsal root dilator fibers. Increasing numbers of in- 

 vestigators have reported, however, that sympathec- 

 tomy completely abolishes reflex vasomotor responses 

 [Jarisch (131), Bacq et al. (23), Schneider (191), 

 Thomas & Brooks (201), Wybauw (229), Bacq et al. 

 (22) and Downman et al. (71)]. 



Of special interest is a paper by Dole & Morison 

 (65) in which they report they were able to confirm 

 Bayliss' observation that a depressor reflex was some- 

 times (in 40 per cent of the cases) accompanied b\' an 

 increase in the volume of a sympathectomized hind 

 limb. However, the increase in volume of the limb re- 

 mained after total denervation of the limlj. Dole & 

 Morison therefore concluded that the vasodilatation 

 sometimes oiiserved after sympathectomy was not of 

 nervous origin. 



Folkow & Uvnas (92) and Lindgren & Uvnas (153, 

 154), directly recording the blood flow in skin and 

 skeletal muscle \essels of cat limbs with cross-circula- 

 tion, so eliminating the disturbing influences of me- 

 chanical and humoral factors, found that sympathec- 

 tomy, acute as well as chronic, inxariably abolished 

 all vasoconstrictor and va.sodilator responses due to 

 occlusion of the common carotids, stimulation of sinus 

 or depressor nerves, and other factors. Sensory de- 

 nervation of the limb, on the other hand, did not 

 influence the vasodilator or vasoconstrictor reflexes 

 studied at all. 



Frumin et al. (93), using a flowmeter, measured the 

 blood flow in the femoral artery of a cross-perfused 

 limb and found that it was greatly increased by de- 

 pressor reflexes produced in different ways. In some 

 experiments they found a slight persisting vasodilator 

 effect even after sympathectomy. This effect was 

 initially attributed to vasodilator activity in the dorsal 

 roots but was later found to he due to a persisting 

 collateral arterial supply to the cross-perfused leg. If 



all collaterals were severed, all vasodilator effects dis- 

 appeared with sympathectomy. 



Celander & Folkow (52J demonstrated that para- 

 sympathetic \asodilator nerves to the tongue or the 

 splanchnic region were not activated by depressor 

 reflexes. Bernthal and co-workers (33) reported that 

 .sympathectomy removed all recognizable chemoreflex 

 vasomotor reactions in the foreleg of the dog even 

 though the dorsal root vasodilator innervation re- 

 mained intact. They concluded that in most dogs sym- 

 pathetic fibers constitute the sole efferent pathway for 

 vascular reflexes originating in the carotid body. 



On the basis of the experimental evidence we pos- 

 sess today, it is accordingly safe to conclude that 

 medullary vasomotor reflexes are mediated solely via 

 variations in sympathetic vasoconstrictor activity. 



INFLUENCE OF C.-^RBON DIOXIDE AND OXYGEN ON 

 SPIN.^L .AND MEDULLARY V.ASOMOTOR NEURONS. Among 



chemical factors influencing the spontaneous activity 

 of the medullary and spinal \asomotor neurons, 

 carbon dioxide is known to be of paramount impor- 

 tance. Increased carbon dioxide tension in the blood 

 reinforces, and decreased carbon dioxide tension 

 reduces the activity as shown by recording the elec- 

 trical activity in sympathetic nerves. In the intact 

 animal, anoxia initially stimulates the vasomotor 

 acti\'ity. 



Bronk et al. (39) oijserved an increase of firing in 

 the inferior cardiac nerves during anoxia which was 

 regarded as secondary to increased firing in the 

 carotid and aortic chemoceptors. Gernandt et al. (97) 

 found that increased carbon dioxide in the Ijlood in- 

 crea.sed the discharge in the splanchnic ner\-e both 

 ijefore and after .section of the sinus and the vagode- 

 pressor nerves. Anoxia led to an increa.se of the po- 

 tentials, pure oxygen inhalation to a decrease, but 

 both these effects disappeared after buffer nerve 

 section. These findings indicate that in the intact ani- 

 mal the vasomotor neurons are more sensitive to the 

 carbon dioxide tension but less sensitive to the oxygen 

 tension than are the chemoceptors. The direct effect 

 of anoxia on the nerve cells is thought to be a de- 

 pressant one [Gellhorn & Lambert (96), Schmidt & 

 Comroe (189)], since after cutting of the buffer nerves 

 anoxia depresses the excitability of the medullary 

 respiratory and vasomotor centers. 



Contrary observations ha\e been made by Alex- 

 ander (6) indicating that anoxia can produce an 

 initial increase in the spontaneous activity of the 

 vasomotor neurons in the deafferented spinal cord. 

 Similarh- the excitabilitx' of vasomotor netirons in 



