IMPAIRED VASODILATORY RESERVE IN DIABETICS WITH AND WITHOUT NEUROPATHY

Several studies have shown that resting blood flow is increased in the diabetic neuropathic foot. It has been proposed that the mechanism in volved is the foss of sympathetic tone which occurs when nerves to per ipheral blood vessels are damaged, resulting in blood vessels being co nstantly dilated. The extent to which further dilatation can be achiev ed when interrupted flow is resumed, we have termed vasodilatory reser ve (VDR). This has not been fully investigated in peripheral blood ves sels of human diabetic subjects. Therefore, we attempted to assess the VDR in diabetic blood vessels by measuring reactive hyperaemia at the ankle. We determined the VDR in 25 neuropathic (ND) and 20 non-neurop athic diabetic (D) patients and compared the finding with those in 17 non-diabetic control subjects (C). Patients and controls were free fro m signs and symptoms of peripheral occlusive arterial disease. Glycaem ic control was assessed by total glycated haemoglobin (GHb). Ankle blo od flow ((Q) over dot) was measured by venous occlusion plethysmograph y. Reactive hyperaemia was induced by occlusion of the ankle at 200 mm Hg for 4 min. Blood flow was then measured at 1 min after deflation of the occlusive cuff to 60 mmHg. The VDR, expressed as the percentage c hange in blood flow from the resting value 1 min after reactive hypera emia, was 12.26%, 32.85%, and 114.75% in the ND, D, and C, groups resp ectively. The difference in mean VDR of diabetic patients and non-diab etic controls was significant (p=0.02). Our present finding indicates an impaired vasodilatory reserve in the ankle of neuropathic and nonne uropathic diabetics, pointing to their inability to increase blood sup ply adequately to the feet after interrupted flow.