Myogenic microvascular responses are impaired in long-duration type 1 diabetes.

Post-ischaemic hyperaemia is a complex physiological response. Peak flow is predominantly an arteriolar myogenic response, whilst viscoelasticity of supplying arteries determines speed of vasodilatation. Impaired post-ischaemic hyperaemia has been described in neuropathic diabetic feet and might predispose to ulceration. However, the relationships of myogenic response and vasodilatation to diabetic control and microvascular complications are unclear. These relationships were therefore investigated using laser Doppler flowmetry to measure the hyperaemic response on the dorsum of the foot after 10 min ischaemia. Twenty control subjects were compared with 55 long-duration Type 1 diabetic patients in groups of uncomplicated, retinopathic and neuropathic patients. Peak flow (median (interquartile range)) was reduced from 1.40 (1.20-1.61) in control subjects to 1.15 (0.80-1.29), 1.08 (0.75-1.26), and 0.95 (0.62-1.29) arbitrary units in the diabetic groups respectively (p = 0.012-0.004). Time to half peak flow was shorter in neuropathic diabetic patients compared with all other groups: 9.5 (7-19), 14.5 (5-25), 12.5 (6-20), and 4 (3-6) s, respectively (p = 0.027-0.011). Neuropathic patients also had the steepest initial slope of vasodilatation. Thus, in long-duration diabetic patients, the myogenic peak post-ischaemic hyperaemic response is impaired, but this impairment is not specifically associated with microvascular complications and was not related to recent blood glucose control. The shortened time to half peak flow and rapid vasodilatation in neuropathic patients is likely to reflect increased rigidity of their arteries.