CONTROL OF PERIPHERAL CIRCULATION 
DR. RODDIE: Yes, that is correct. That was seen on the fingers 
of patients with Raynaud's disease, but they were never able to 
demonstrate this on normal people. This question has been pursued 
quite hotly ever since because it seemed unreasonable that this type 
of fibre should be confined to these patients. 
DR. HEMINGWAY: Well, my point is, will the release of brady- 
kinin, which has been used as evidence for the existence of vaso- 
dilator nerves, explain that? 
DR. RODDIE: I suppose it is possible, if these patients with 
Raynaud's disease were rather anxious people and were upset by 
the procedures that Sir Thomas first subjected them to. This could 
account for a vasodilatation on the normal side and the absence of a 
vasodilatation on the nerve blocked side. 
DR. HEMINGWAY: Well, the other thing lam tiding to get at is 
this; is it necessary to postulate the existence of vasodilator fibres 
if you have the bracfykinin mechanism? 
DR. RODDIE: No, but there has been this difficulty of what to 
call these fibres. A fibre is a vasodilator if you think that there is 
only one intermediary. Now, it is veiy difficult to prove that there is 
only one intermediary. I, personally, think it would be better not to 
call these fibres to skin "vasodilator", but it is hard to think of a 
concise alternative. 
DR. HEMINGWAY: It is an old, old argument, you know. /\11 the 
evidence is rather indirect for the existence of the vasodilator. 
DR. RODDIE: I think so. Of course, this criticism applies to 
the muscle vasodilators, too. One thinks that the acetylcholine re- 
leased at the nerve ending acts directly on the blood vessels and it 
is possible that acetylcholine acts on some cell, which in turn pro- 
duces an agent which acts on blood vessels. 
MR. EAGAN: I believe the term you used was vasodilator 
mechanism. 
DR. RODDIE: Yes, but that sometimes confuses people, too. 
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