Toms S L, Cooke E D
Department of Medical Electronics, St. Bartholomew's Hospital, London.
Int Angiol. 1995 Mar;14(1):74-9.
Little information is available on the functioning of the arteriovenous anastomoses (AVA's) and their involvement in the pathophysiology of cold sensitivity and abnormal thermoregulation in scleroderma. Twenty-four patients with scleroderma and twenty two control subjects were included in an investigation to test the hypothesis of abnormal functioning of AVA's. Cutaneous microcirculatory flow was measured using non-invasive instrumentation (infrared photoplethysmography, laser Doppler flowmetry and thermography) which allowed microcirculatory flow to be characterized at different levels, before and after warming of the hand at 40 degrees C for 5 minutes. The sclerodermics showed significantly reduced microcirculatory flow and hand temperatures throughout the investigation indicating the presence of organic vascular structural changes. However, the most striking finding was the reduction in microcirculatory volume in the control hand in contrast to the increase in the sclerodermic hand, on warming. We propose that the decrease in microcirculatory volume in the controls is due to a form of "steal" phenomenon where dilatation of the AVA's allow the shunting of blood away from the capillaries directly into the deeper cutaneous veins. The absence of this response in the sclerodermic group suggests the failure of the AVA's to open on warming. It is likely that the morphological vascular changes may be only partly responsible for the abnormal functioning of the AVA's and that dysfunction of the peripheral nervous system, as a consequence of microangiopathy, may also be a contributory factor.