Arachidonic acid metabolism and regulation of blood flow: effect of indomethacin on cutaneous and subcutaneous reactive hyperaemia in humans

Abstract

Summary. The role of locally formed vasodilator prostaglandins (PGs) in the vascular relaxation response to short‐lasting arterial occlusion (reactive hyperaemia) in human cutaneous and subcutaneous tissue was investigated. The finger was chosen to represent cutaneous tissue, and its blood flow was determined using venous occlusion plethysmography; thigh adipose tissue represented subcutaneous tissue, and blood flow here was measured with an isotope clearance technique. Flow rates were determined in the basal state and during the hyperaemic phase following a period of arterial occlusion. The procedure was repeated after administration of the PG synthesis inhibitor indomethacin, given in a dose of 1·5 mg/kg.In neither cutaneous nor subcutaneous tissue was the basal blood flow affected by indomethacin. In the finger, an increase in blood flow developed after the end of the arterial occlusion, reaching a peak value at 65 s of about 65 ml‐1 100 ml tissue min‐1. Indomethacin reduced the amplitude of this post‐occlusive increase to about 45 ml 100 ml‐1 min‐1, but did not change its duration. The total reactive hyperaemia in the finger was reduced by more than 50% following indomethacin. The subcutaneous tissue likewise showed an increase in blood flow following release of the arterial occlusion. This increase was not affected by indomethacin, in terms of either amplitude, duration or total reactive hyperaemia.From these data, we conclude that short‐lasting arterial occlusion leads to formation of a vasodilator PG that plays a decisive role in the subsequent vascular smooth muscle relaxation response in human cutaneous tissue. A similar chain of events does not take place in ischaemic subcutaneous vascular tissue.