Ninety-three patients with treatment-resistant venous ulcers were included in a multicentre randomized trial to compare cadexomer iodine and the standard treatment used in each centre combined with compression bandages, in healing venous ulcers. The mean duration of ulcers before the trial was more than 2 years. With standard treatment the mean ulcer size increased slightly during the 6-week trial whereas with cadexomer iodine the ulcer size was significantly reduced. Cadexomer iodine was more effective than standard treatment for reduction of pain, removal of pus and debris, removal of exudate, stimulation of granulation and reduction of surrounding erythema. Bacterial infection of ulcers increased or did not change during treatment with the standard therapy whereas cadexomer iodine significantly reduced infection with Staphylococcus aureus, Pseudomonas aeruginosa and other pathogenic organisms. A correlation was seen between the time taken to reduce or eliminate infection with Staphylococcus aureus and rate of ulcer healing. Four patients complained of transient pain in the ulcer after application of the cadexomer iodine. It is concluded that cadexomer iodine increased the rate of healing of infected chronic venous ulcers.

No abstract

The role of the endothelium to influence smooth muscle contraction in normal and varicose veins was investigated in vitro using saphenous vein preparations obtained at vascular surgery. Paired control and endothelium-denuded rings were tested simultaneously and contracted with noradrenaline (10(-9)-10(-4) M). Identical experiments were also performed on sheep femoral veins and arteries. Noradrenaline induced maximal tension was 30% lower in varicose compared to normal veins. In normal veins removal of endothelium significantly reduced the maximal response to noradrenaline by 40% whereas in varicose veins no significant reduction could be seen. In the sheep femoral vein removal of the endothelium also resulted in decrease of noradrenaline-induced contraction. It can be concluded that in the human saphenous vein the endothelium has a contraction facilitating effect in response to stimulation with noradrenaline. In varicose veins the endothelial-mediated enhancement of noradrenaline-induced vasoconstriction is reduced probably because of endothelial damage. This observation may be of importance in the pathogenesis of varicose veins.

ST 1059, the pharmacologically active metabolite of midodrine, is a powerful vasoconstrictor compound, acting by stimulation of alpha-receptors. It elicited 80% of noradrenaline-induced contraction of human veins.

Specimens from the proximal and distal parts of saphenous vein of 16 patients undergoing stripping operations for varicose veins were investigated with pharmacological technique and electron microscopy. The ultrastructural investigation showed a venous wall with increased connective tissue elements such as collagen fibres. In parts endothelial damage could be observed. These changes were about equally frequent in specimens from the proximal and distal great saphenous vein. The pharmacological study showed reduced maximal contraction of varicose veins compared to controls. Moreover there was a slightly higher maximal tension (contraction per unit trans-sectional area) in specimens from the lower leg, compared to the thigh. This means that there is functional disturbance of the smooth muscle function in varicose veins, and other structural elements show significant alterations such as connective tissue and endothelial cells.