Comportamento della eNOS e dell'iNOS nella genesi e mantwnimento delle ulcere venose degli arti inferiori

Chronic venous insufficiency (CVI) and venous ulcers in the lower areas are widespread problems with a prevalence of 1% - 2% in the western population. The pathophysiology of this pathological manifestation is not yet fully clarified and it can be assumed that a multifactorial genesis should be considered. Certainly the high pressure values ​​in the peripheral venous system, the defective valves in the capillary network, the increase in permeability and capillary neogenesis (discharge of liquids in the extracellular compartment - + edema), the discharge of fibrinogen and the subsequent formation of a pericapillary fibrin cuff are the most important mechanisms related to hypoxia and skin ischemia and represent the first step for the formation of skin ulcers of the lower areas. In addition, following ischemic events, white blood cells can cause damage to tissues through the release of free radicals, proteolytic enzymes and cytokines. Furthermore, several authors hypothesize a hypothesis of 'white cell entrapment' responsible for endothelial damage which translates into additional damage to microcirculation. NO plays a fundamental role in the circulatory system, albeit in different ways. In fact, under physiological conditions, O is produced enzymatically in small quantities and for a short period of time by endothelial cells (eNOS) and by nitroxyergic neurons that innervate the vessels (nNOS); under pathological conditions the production of NO is inducible in macrophages (iNOS) from bacterial LPS and / or from the cytokines of white blood cells (7-8) and is produced in large quantities and for a long period. The result of its action is a massive vasodilation, which leads to a microcirculatory stasis.