The microvascular response of foot skin to minor thermal injury and the skin of the anterior abdominal wall to injury from a needle was assessed by laser Doppler flowmetry in 23 patients with type I diabetes and 21 healthy control subjects. After minor thermal injury mean (SD) maximum skin blood flow was significantly lower in the diabetic group than the control group (0.53 (0-11) v 0-72 (0.10) V, in arbitrary units of flow, respectively, p<0001) and was negatively correlated with the duration of diabetes (r= -0-60; p<0-01). After needle injury a similar pattern of impairment was seen, the peak flow value recorded being significantly lower in the diabetic group than the control group (0.28 (0-10) v 0-41 (0-09) V, respectively; p<0-001) and also negatively correlated with the duration of diabetes (r=-0-61; p<0-01). There was a significant relation between the response obtained at the two sites of injury in the diabetic group (r= + 0-72, p<0O001) but not in the control group. The impairment in response was not related to diabetic control and was not explicable in terms of a reduction in superficial skin capillary density.

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It was first shown by Ludwig in 1851 that stimulation of the chorda tympani nerve or of the cervical sympathetic chain evoked a secretion of saliva from the submaxillary gland of the cat. Claude Bernard (1858) later showed that, whereas parasympathetic stimulation produced a concomitant vasodilatation, sympathetic stimulation produced vasoconstriction. It was also observed subsequently that a vasodilatation often followed this constriction (Carlson, 1907). Heidenhain (1872) made the interesting observation that although a small dose of atropine completely blocked the secretion produced by stimulation of the chorda tympani nerve, the intense associated vasodilatation was practically unaffected. The latter experiment was performed on dogs but the same phenomenon also occurs in cats (see Burgen & Emmelin, 1961).For many years the view was generally held that there were separate secretory and vasomotor nerve fibres in both the parasympathetic and sympathetic nerves to this gland. The existence of dilator nerve fibres was first challenged by Barcroft and his colleagues (Barcroft & Piper, 1912;Barcroft, 1914) as a consequence of their experiments on the relation between metabolic activity, secretion and blood flow in the submaxillary gland. From these experiments Barcroft (1914) concluded that the vasodilatation which is associated with sympathetic nerve stimulation is entirely secondary to the secretory metabolism. He was somewhat more cautious in dismissing the presence of vasodilator fibres in the chorda tympani nerve, stating: 'It is not impossible that under normal circumstances dilatation may be instituted by dilator fibres and maintained by metabolic products.' Bayliss (1923), who held the view that parasympathetic dilator nerve fibres were responsible for this dilatation, pointed out that although Barcroft's measurements on oxygen consumption and vasodilatation showed that these activities increased at the same time, they

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