1136 



HANDBOOK OF PHYSIOLOGY 



NEUROPHYSIOLOGY II 



vessels are devoid of nervous regulation. The coronary 

 blood flow would consequently be regulated only by 

 the metabolic need of the heart. 



(■) Skin. Bill bring & Burn (46) have claimed that, 

 in contrast to other cutaneous areas, the vessels of the 

 ear have a sympathetic vasodilator nerve supply since 

 stimulation of the cervical sympathetic caused a slight 

 increase in the volume of the ear in the ergotaminized 

 dog. Folkow and co-workers (82), however, also 

 stimulating the cervical sympathetics, were unable to 

 convert a vasoconstrictor response in the ear into a 

 vasodilator response, even with the use of huge doses 

 of ergotamine or Dibenamine. A possible explanation 

 of the divergent results is the different techniques used 

 for recording the blood flow. Uvnas el al. measured 

 the venous outflow from the distal part of the ear 

 while the plethysmographic technique of Biilbring & 

 Burn revealed volume changes not only in cutaneous 

 areas but also in the muscles at the base of the ear. 



d) Intestines. The assumption that the splanchnic 

 nerves carry vasodilator fibers to the intestines of the 

 dog and cat is based on the observation of Biilbring & 

 Burn (46) that stimulation of a splanchnic nerve 

 causes an increase in the volume of an intestinal loop 

 enclosed in a plethysmograph. Folkow et al. (83) con- 

 firmed that stimulation of a splanchnic nerve was 

 able to induce a slight increase of the intestinal venous 

 outflow in an ergotaminized cat. The latter writers 

 attributed the increase in blood flow not to activation 

 of vasodilator nerves, but to changes in the peripheral 

 vascular resistance caused by relaxation of intestinal 

 muscle 



From the available experimental evidence dis- 

 cussed above, Uvnas et al. concluded that a sympa- 

 thetic vasodilator supply in the dog and cat was pres- 

 ent in the striated muscles and possibly the heart, 

 but not in the intestines and the skin. Figure 10 illus- 

 trates the present writer's view of the central and the 

 peripheral distribution of the sympathetic vasodilator 

 outflow. 



Cannon et al. (48) recently questioned whetiier all 

 va.sodilator eflfects observed on activation of the sym- 

 pathetic nerves might not be due to a decrease of 

 vasoconstrictor tone since direct stimulation and re- 

 flex activation of the sympathetic outflow might some- 

 times be accompanied by poststimulatory inhibition 

 of the tonic discharge in postganglionic fibers. A 

 similar poststimulatory inhibition was observed by 

 Bronk et al. in the inferior cardiac nerves after hypo- 

 thalamic stimulation. Tiie observations are interest- 



ing, but their physiologic implications are quite un- 

 known. 



The occurrence of poststimulatory inhibition of the 

 tonic sympathetic cardiovascular discharge does not 

 warrant the a.ssumption that no vasodilator nerves 

 exist. It is not possible, for instance, to class as post- 

 stimulatory inhibition those vasodilator responses in 

 skeletal muscle to intracerebral stimulation that are 

 potentiated by physostigmine and completely abol- 

 ished by atropine, or that can be elicited by post- 

 ganglionic stimulation after degeneration of pre- 

 ganglionic fibers. 



CHEMic.'iiL TRANSMISSION, a) Skeletal muscles. As long as 

 all sympathetic postganglionic neurons were believed 

 to be adrenergic and epinephrine to be the sole trans- 

 mitter substance at sympathetic postganglionic nerve 

 terminals, it was logical to assume that epinephrine 

 was also the transmitter at sympathetic vasomotor 

 nerve terminals, both vasoconstrictor and vasodilator. 

 After the discovery of cholinergic fibers in the sympa- 

 thetic postganglionic outflow [Dale & Feldberg (78)], 

 it was not surprising, however, to learn that in the dog 

 the sympathetic vasodilator nerves to facial muscles 

 [von Eulcr & Gaddum (211)] and to muscles of the 

 hind legs [Biilbring & Burn (44)] were regarded as 

 cholinergic. These claims were based on the fact that 

 in both areas stimulation of the sympathetic nerves 

 caused contractions of muscles deprived of somatic 

 motor innervation. In the hind legs of the dog, the 

 vasodilator effects were augmented ijy physostigmine 

 and blocked by atropine. Since in tiie hind legs of the 

 cat, vasodilator responses occurred only in ergot- 

 aminized animals and were not significantly in- 

 fluenced by physostigmine and atropine, cat vasodila- 

 tor fibers were believed to be adrenergic, epinephrine 

 being the chemical mediator. 



Following the demonstration by Roscnblueth & 

 Cannon (184) that the abdominal sympathetic nerves 

 contained both adrenergic and cholinergic vasodilator 

 fibers, Biilbring & Burn (45) demonstrated cholingeric 

 vasodilator fibers to the hind legs of the cat since they 

 observed a feeble Sherrington phenomenon in a de- 

 nervated leg on stimulation of the abdominal sympa- 

 thetic chain. A similar observation had already been 

 made in 1933 by Hinsey & Cutting (125). 



Uvnas et al. (gi, 92) reached the conclusion that 

 the sympathetic vasodilator nerves to the skeletal 

 muscles of the cat were exclusively cholinergic since 

 the vasodilator responses in the hind legs to stimula- 

 tion of the abdominal sympathetic chain and to 

 intracerebral stimulation were potentiated jjv phvso- 



