Impaired vasodilatory reserve in diabetes with and without neuropathy - abstract

ABSTRACT

Several studies have shown that resting blood flow is increased in the diabetic neuropathic foot, It has been proposed that the mechanism involved is the loss of sympathetic tone which occurs when nervesto peripheral blood vessels are damaged resulting in blood vessels being constantly dilated. The extent to which further dilatation can be achieved when interrupted flow is resumed we termed vasodilatory reserve (VDR). This has not previously been investigated. We, therefore, attempted to assess the VDR in diabetes' blood vessels by measuring reactive hyperaemia at the ankle. The VDR was determined in 23 neuropathic (ND), and 16 non-neuropathic diabetic (D) patients and compared with 16 non-diabetic control subjects (C). Patients and controls were free from signs and symptoms of peripheral occlusive arterial disease. Glycaemic control are assessed by glycosylated haemoglobin levels. Ankle blood flow (Q) was measured by venous occlusion plethsmography. Reactive hyperaemia was induced by occlusion of the ankle at 200 mm Hg for 4 minutes. Blood flow was then measured at 1 minutes deflation of the occlusive cuff to 60 Hg. The VDR is expressed as the precentage change in blood flow from the resting value 1 minute after reactive hyperaemia. VDR was 14.49 percent, 20.8 percent and 114.75 percent in the ND, D and C groups respectively. Our present finding indicated and impaired vasodilatory reserve in the ankle of neuropathic and non-neuropathic diabetes pointing to their inability to adequately increase blood supply to the feet after interrupted flow(AU)