THE ROLES OF TURBULENCE AND VASA VASORUM IN THE ETIOLOGY OF VARICOSE-VEINS

Noradrenaline can dilate a canine lateral saphenous vein which at the time is constricted by noradrenaline. It does so when it is released from the vasa vasorum network of the constricted vein. By filling a limited section of the network of a normal, tonically constricted vein with endogenous noradrenaline it is possible to dilate the vein locally, in effect creating an acute experimental varicosity. These findings have led to the proposal that human varicosities are an active response of the vein to endogenous noradrenaline released from sections of its vasa vasorum network. The noradrenaline involved is part of the circulating overflow derived from normal adrenergic nerve activity. A bout of turbulence in the vein lumen is proposed as the trigger which causes a reflux of hypoxic blood and the endogenous noradrenaline in it from the vein lumen to the vasa. The size and shape of the varix reflects the mosaic pattern of a vein's vasa vasorum network. The site of the varicosity is determined by the location in the vein lumen of the bout of turbulent non-laminar flow.