The origin and the progression of varicose veins.
It is proposed that pathological varicosities begin as acute dilator responses of normal veins to noradrenaline released from the vasa vasorum of the vein; the noradrenaline is part of a circulating pool formed by overflow following adrenergic nerve activity. In health, a minimal quantity of noradrenaline routinely flows by reflux to the vasa where it has a negative feedback, venodilator effect. However, when the volume of reflux becomes excessive, the noradrenaline in it abolishes venoconstrictor tone, thereby creating a varicosity. Excessive venous reflux over a short period causes no significant hypoxic damage to the vein wall or any other tissues and any damage associated with it regresses when the excess reflux ceases. However, if excessive reflux is persistent then a time comes when irreversible hypoxic structural changes occur in the vein wall and in other tissues affected by the reflux. The structural pathology associated with varicose veins reflects the effect of the long-term tissue hypoxia associated with that condition.
Crotty
T P
TP
Anatomy Department, University College, Cork, Ireland.
D000818:Animals; D006801:Humans; D000860:Hypoxia / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D008954:Models, Biological; D009638:Norepinephrine / Q000502:physiology; D014648:Varicose Veins / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D014651:Vasa Vasorum / Q000503:physiopathology; D014664:Vasodilation / Q000502:physiology
D009638:Norepinephrine