RODDIE, I. C. 
DR. HENSEL; Yes. I think that in the experiment with mental 
arithmetic there is quite strong evidence for a non-cholinergic 
vasodilator mechanism. GoUenhofen found in many cases by giving 
very high doses of atropine the effect is only very slightly decreased 
if at all. So I think the amount of non-cholinergic vasodilator fibres 
might be quite considerable. 
DR. RODDIE: Yes, I think this varies quite a lot from stimulus 
to stimulus because we found an enormous variation in the reduction 
in the vasodilatation during emotional stress that we could obtain by 
atropine. Sometimes it was negligible with the lesser degrees of 
fright, but usually when we had genuine fear it was larger. 
DR. HENSEL: It is difficult with your method; you can only call 
the ambulance car one time' 
DR. MINARD: I would like to ask what the effect of norepineph- 
rine is on blood vessels to muscle. 
DR. RODDIE: If you give norepinephrine intra-arterially to one 
forearm, after a transient increase in flow in the forearm, vasocon- 
striction occurs, and this persists as long as the infusion lasts. 
DR. MINARD: I am interested then in how this blocking agent 
acts. You say you block the vasodilator effect by means of this 
blocking agent? 
DR. RODDIE: Yes, bretylium tosylate is now being used for 
hypertension. It is taken up specifically by the noradrenergic nerve 
fibres where it acts as a local anaesthetic. With sufficient dosage, 
it apparently will block practically all fibres but with the right 
critical dosage, it blocks mainly the adrenergic fibres. It is quite a 
useful tool and is the best sympathetic adrenergic block that we 
have used. It does not block the effect of circulating epinephrine or 
norepinephrine, just the nerve fibres. 
DR. HEMINGWAY: The evidence for vasodilator fibres goes 
way back to the time of Thomas Hood. In a blocked nerve, in an area 
where the nerve is blocked, the blood flow is less than as a result 
of local heating. 
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