CENTRAL CARDIOVASCULAR CONTROL 



II35 



highest that fails to produce any abnormal post- 

 stimulatory prolongation of the vasoconstrictor re- 

 sponses, Folkow concluded that the physiologically 

 occurring peripheral vasomotor discharge rate ex- 

 ceeded 6 to 8 impulses per sec. only in exceptional 

 cases. 



The direct recordings of Bronk et al. are strikingly 

 consistent with the indirect observations made by 

 Folkow et al. and Girling. Maximal effects of stimula- 

 tion may appear at impulse frequencies of around 10 

 per sec. and normal effector activity maintained with 

 I to 3 impulses per sec, although this may require 

 supramaximal stimulation and simultaneous dis- 

 charge of all postganglionic fibers. 



The fact that all blood vessels have a vasoconstrictor 

 innervation does not mean that vasoconstrictor tone 

 is evenly distributed in the various vascular beds. 

 The general opinion is that this tone is especially pro- 

 nounced in the splanchnic vessels, but its existence in 

 cutaneous and muscle vessels is evident from the 

 simple fact that the blood flow increases considerably 

 in those vascular areas with sympathectomy. In other 

 vascular areas, such as the cerebral region, vasocon- 

 strictor tone is considered to be slight. 



It is not known whether the varying degrees of 

 tone in different vascular areas may be due to varying 

 frequencies of the vasoconstrictor discharge thereto 

 or to other factors. Celander & Folkow (53) have 

 pointed out that quantitative differences in the vaso- 

 constrictor innervation apparently exist between, for 

 instance, cutaneous and muscle vessels. Stimulation 

 of the abdominal sympathetic chain increased the 

 peripheral resistance 9.5 to 10 times in the muscle 

 ves.sels, but up to 100 in the cutaneous vessels. In the 

 opinion of Celander & Folkow, these quantitative 

 differences in the responses were probably due to a 

 more abundant va.soconstricior innervation to the 

 cutaneous than to the mu-scle vessels. 



Sympathetic Vasodilator Nerves 



Electrical stimulation of sympathetic fibers usually 

 brings about vasoconstriction in the innervated area, 

 even if the stimulated outflow contains both vaso- 

 constrictor and vasodilator fibers, since the action 

 of the former predominates. By special techniques, 

 such as the use of stimuli of certain characteristics and 

 physostigmine, it may be possible to produce a vaso- 

 dilator effect [Biilbring & Burn (44), Folkow & Uvnas 

 (90, 91)]. The vasodilatation obtained is, however, 

 usually slight and transient. Better results are yielded 

 bv observations on animals treated with erafotamine 



or other sympatholytic drugs. If the sympathetic 

 outflow contains vasodilator fibers, electrical stimula- 

 tion is then able to produce manifest vasodilatation, 

 because when the action of the released vasoconstrictor 

 transmitter is blocked that of the vasodilator trans- 

 mitter is unmasked. 



Uvnas and associates (75, 76, 149, 152) have lately 

 succeeded in activating sympathetic vasodilator nerves 

 in cats and dogs by topical stimulation in the brain, 

 using the Horsley-Clarke technique which allows ob- 

 servations without previous administration of sympa- 

 thicolytic agents. 



PERIPHERAL DISTRIBUTION, a) Skeletal muscles. Sympa- 

 thetic vasodilator nerves were shown to run to the 

 muscles of the hind legs of the dog and cat by Biilbring 

 & Burn (44), Folkow & Uvnas (90, 91), Frumin et al. 

 (93), Youmans et al. (230) and po.ssibly of the hare 

 [Biilbring & Burn (47)] and fox (unpublished ob- 

 servations). Other animals, e.g. the rabbit and mon- 

 key, were claimed to lack such nerves. 



Barcroft and co-workers (25) noted an increase of 

 the human forearm blood flow during fainting. Since 

 the arterial pressure fell at the same time and the blood 

 flow was shown to be greater in a normal forearm than 

 in a nerve-blocked forearm, sympathetically-mediated 

 active vasodilatation was suggested to occur in tlie 

 normal forearm. 



b) Coronary vessels. The sympathetic outflow to the 

 heart is commonly assumed to contain coronary dila- 

 tor fibers since electrical stimulation of the stellate 

 ganglion or of the cardiac nerves has been observed 

 to cause an increase in the coronary flow [Gollwitzer- 

 Meier & Kriiger (loi), Greene (108), Katz & Jochim 

 (138), Gregg & Shipley (no), VVinbury & Greene 

 (225) and others]. Circumspection is required, how- 

 ever, in the interpretation of these observations, for 

 stimulation of the sympathetics to the heart brings 

 about acceleration and an increase of the contractile 

 force of the heart and hence an increase in the metab- 

 olism of the heart muscles. This in itself will increase 

 the coronary blood flow, probably due to the ac- 

 cumulation of metaijolites with a vasodilator action. 

 Gregg & Shipley (iio) reported that electrical stimu- 

 lation of the sympathetic nerves to the heart produced 

 an increase in the coronary flow without a con- 

 comitant acceleration of the heart. This observation 

 suggests that sympathetic vasodilator fibers run to the 

 coronary vessels. Katz & Jochim (138) are alone in 

 assuming that cholinergic vasodilator fibers to the 

 coronaries run in the vagus. An extreme view is held 

 by Eckenhoff (73) who claims that the coronary 



