CENTRAL CARDIOVASCULAR CONTROL 



'37 



stigmine and abolished by atropine, and since acetyl- 

 choline appeared in the perfusate from physostig- 

 minized legs, as had previously been shown to occur 

 in the dog. 



h) Coronary vessels. The sympathetic coronary vaso- 

 dilator nerves are conventionally assumed to be 

 adrenergic. It is indisputable that epinephrine in- 

 creases the coronary blood flow, even on intracoronary 

 injection. Moreover, many workers have demon- 

 strated that stimulation of the stellate ganglion or of 

 the cardiac sympathetic nerves increases the coronary 

 output. Atropine does not abolish this eflFect. However, 

 epinephrine as well as sympathetic stimulation in- 

 creases the activity of the heart. Consequently, it 

 cannot be ruled out that the increased blood flow may 

 be secondary to the increased muscle metabolism 

 as it is in the skeletal muscle during exercise. 



Acetylcholine dilates the coronary arteries [Ecken- 

 hoff et al. (74), Folkow et al. (84), and the sympathetic 

 nerves carry cholinergic fibers to the heart in the cat 

 and dog [Gollwitzer- Meier & Kriiger (loi), Folkow 

 et al. (81)]. These observations suggest that the coro- 

 nary vasodilator fibers — if such fibers exist — may be 

 cholinergic. 



c) Conclusion. No positive evidence has been pre- 

 sented to show that epinephrine is a nervous mediator 

 of vasodilator effects. Until the existence of adrenergic 

 vasodilator fibers has i)een experimentally established, 

 they are better omitted from the discussion. [This 

 question has been discussed in greater detail by 

 Folkow & Uvnas (92).] 



PHYSIOLOGIC PROPERTIES AND IMPULSE FREQUENCV. 



No direct ob.servations have iieen made regarding the 

 diameters and transmission properties of fibers in the 

 sympathetic vasodilator outflow since it has not yet 

 been possible to identify or isolate such fillers. It is 

 plausible by analogy to assign the preganglionic fibers 

 to group B and the postganglionic fibers to group C. 



Maltesos & Schneider {160, 161) stimulated the 

 abdominal sympathetic chain in dogs and observed 

 an increased blood flow in the femoral vein. A con- 

 centration of the chronaxie values for vasodilatation 

 around figures between o. i and 6 msec, was attributed 

 to the presence of vasodilator fibers of varving di- 

 ameters. 



Experimenting on cats, Folkow & Gernandt (85) 

 reported an increased outflow of impulses recorded 

 from fine strands of the peroneal nerve running to 

 the muscles of the hind limb, closely associated in time 

 with the vasodilator effect in the muscle caused by 

 hypothalamic stimulation. This discharge was as- 



sumed to reflect the activity in small postganglionic 

 nonmyelinated sympathetic vasodilator fibers. The 

 voltage of the spikes was too low to allow any detailed 

 analysis of the discharge. 



Studies on the relation between the impulse fre- 

 quency and the degree of vasodilatation were carried 

 out by Folkow (80) in the hind-leg muscles of the 

 cat by stimulating the abdominal sympathetic chain 

 after administration of dihydroergotamine to block 

 the vasoconstrictor eflTects of the stimuli. It was found 

 that dilatation already occurred at a stimulation rate 

 of I per sec. With a frequency of 6 per sec. the dilata- 

 tion was very marked with more than a fivefold in- 

 crease of the blood flow, while at 1 2 per sec. a maximal 

 vasodilator response appeared. Atropine completely 

 blocked the vasodilatation, thus proving it to be due 

 to activity in cholinergic vasodilator nerves. 



The meager experimental evidence available con- 

 cerning the physiologic properties of the sympathetic 

 vasodilator nerves accordingly suggests properties 

 resembling those of the vasoconstrictor nerves. The 

 physiologic firing rate can be assumed to be rather 

 low, up to about 10 per sec. As far as is known, no 

 tonic discharge occurs in the sympathetic vasodilator 

 outflow. 



Parasympalhetic I'asoddator \erves and Cardiac Vagus 



PERIPHERAL DISTRIBUTION. Parasympathetic va.sodila- 

 tor nerves are considered to run in the chorda tympani 

 to the tongue and glands of the oral cavity, and in the 

 sacral autonomic outflow to the genitals and, possibly, 

 to the urinary bladder and rectum. Investigations 

 recently reported by Hilton & Lewis (122-124) show, 

 however, that the vasodilatation observed in the sub- 

 lingual gland on stimulating the chorda tympani 

 probably is produced by bradykinin formed by the 

 activated gland. There is no need to postulate a sepa- 

 rate vasodilator innervation. As regards the tongue, 

 stimulation of efferent fibers in the chorda tympani 

 elicits a very marked increase in the venous outflow. 

 Since this vasodilator effect cannot be ascribed to in- 

 creased metabolic activity, one has to a.ssume that it 

 is due to acti\'ation of va.sodilator fibers. 



Vasodilator fibers are claimed to run in tiie facial 

 nerve [Cobb & Lennox (60)] and the trigeminal nerve. 

 The reports on the course and origin of the.se fillers 

 are unreliaijle. It is not clear whether they are efferent 

 fibers, or afferent fibers capable of antidromic trans- 

 mission of vasodilator impulses. Vagal vasodilator 

 fibers are said to supply the liver blood vessels [Gins- 

 burg & Grayson (gg)]. 



