CONTROL OF PERIPHERAL CIRCULATION 
thought to cause reflex vasoconstriction. There is evidence that al- 
terations in the activity of stretch or baroreceptors in the low pres- 
sure area of the intrathoracic vascular bed may be responsible for 
some of the changes in the vasoconstrictor tone (Roddie and Shep- 
herd, 1958), but this part of the problem is quite complex and there 
is not time to discuss it today. 
Vasodilator Fibres 
The first evidence that human skeletal muscle had a vasodilator 
innervation was provided by BarcroftandEdholm (1945). They found 
that vasodilatation occurred in the forearm durningfainting(Fig.3). 
The conclusion that the vasodilation in the normal forearm was 
actively excited was based on a comparison of the average levels of 
flow in nonnal and nerve-blocked forearms during the faint; the 
flow in the normal arm rose to a higher level than that in the nerve- 
blocked arm. Though this evidence is highly suggestive, it is not 
absolutely conclusive since the observations on the normal and 
nerve-blocked forearms were not made simultaneously in the same 
subject. However, evidence has since been found that vasodilation 
in muscle is a constant feature of the vasovagal syndrome (Anderson, 
Allen, Barcroft, Edholm, and Manning, 1946). 
It seemed unlikely that a potent vasodilator system should exist 
just to facilitate fainting so a vigorous search was made to find a 
stimulus which would excite these fibres under more normal phys- 
iological conditions. As mentioned before we could find no evidence 
that these fibres were involved in bare receptor reflexes. Another 
incentive to search for a stimulus was the abundant evidence for 
these fibres supplying muscle in other experimental animals. In the 
cat and dog, cholinergic vasodilator innervation of skeletal muscle 
is well established and the central connections and efferent distri- 
butions of these fibres has been extensively studied (Uvnas, 1954). 
It was found that they played no part in either chemoreceptor or 
baroreceptor reflexes but the exact nature of the physiological re- 
flex stimulus was not obtained. Abrahams and Hilton (1957) have 
recently shown that stimulation by electrodes implanted in those 
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