1. Hand blood flows in healthy young men and women and in patients with anorexia nervosa were measured in a warm environment by using venous occlusion plethysmography. The mean core temperature of each of the three groups was similar, but the male control subjects and the anorexic patients had significantly higher peripheral blood flows than the female control subjects. 2. Blood flows were determined in the hand after 6 min localized cooling of it at varying temperatures. The female control subjects and the majority of the anorexic patients had blood flows which were similar for a given temperature, and lay between the higher values of the male control subjects and the low values of the remaining anorexic patients. 3. Those patients whose vascular responses to cold were exaggerated were characterized clinically by severe and persistent signs of ischaemia of the extremities during subsequent rehabilitation, unlike the majority of patients whose peripheral circulation rapidly improved. 4. Cold thermal stimuli evoked marked falls in blood flow of the contralateral (non-cooled) hand in the male and female control subjects, but these responses were attenuated or absent in the anorexic patients. An altered set-point for vasomotor thermoregulation in anorexia nervosa could explain these findings. 5. Plasma and whole-blood viscosity and erythrocyte deformability measured in a sample of the patients studied were similar to the values obtained from a sample of the control subjects. 6. It was concluded that the cutaneous vasoconstrictor responses to cold in the majority of the anorexic patients studied were quantitatively normal. The mechanism of the response, however, was different in that the vessels themselves were unusually reactive to cold. Increased cuteneous vasoreactivity to cold could contribute to the severe peripheral hypoperfusion observed in some anorexic patients.

1. The response of hand blood flow to acute insulin-induced hypoglycaemia was measured in normal subjects in whom vasomotor tone had been released physiologically by body heating, anatomically by unilateral nerve block and pharmacologically by unilateral intra-arterial infusion of bretylium tosylate or phenoxybenzamine. Five patients who had undergone unilateral cervical sympathectomy were also studied. 2. Under these conditions the usual increase in hand blood flow associated with acute hypoglycaemia was converted into a decrease except during complete unilateral α-adrenergic blockade when hypoglycaemia produced no change in hand blood flow. 3. The possible mechanisms responsible for the vasodilatation associated with hypoglycaemia are discussed. 4. The results suggest that release of vasoconstrictor tone, rather than activation of specific vasodilator mechanisms (neurogenic or humoral), is the principal means whereby acute hypoglycaemia produces increased blood flow in the hand.