[The vasa vasorum of the arteries]

Nourishment of arteries is accomplished by diffusion from the lumen of the vessel and from vasa vasorum. Most normal arteries have an extensive network of vasa in the adventitia that arise from branch points of parent arteries. When the thickness of arteries exceeds the ability of simple diffusion of nutrients from the lumen (larger muscular of atherosclerotic arteries), vasa extend into the media and intima. Vasa in the intima-media arise predominantly from adventitial vasa, but can arise from the lumen in vascular grafts and recanalized arteries after thrombosis. Vasa respond to vasoactive stimuli, and can regress after they vascularize arterial grafts and in response to regression of the atherosclerotic lesions. Therefore, vasa can increase blood flow to the artery wall by dilation of existing arteries or by formation of new vessels (neovascularization). Conversely, vasa can reduce blood flow to the artery wall by active constriction or by regression (involution) of existing vasa. The pathophysiological significance of vasa vasorum in normal and diseased arteries is related to their structure. Vasa in the intima-media are thin-walled endothelial cell tubes with thin or absent medial smooth muscle cells. Therefore, they are prone to collapse and rupture in response to arterial pressure, mechanical forces in the artery, necrotic substances found in diseased arteries, and vasospasm. Vasa also provide the artery with a vast absorptive endothelial surface that may have important implications for arterial lipid kinetics, and delivery and removal of neurohumoral agents from the artery wall. These properties have lead to speculation about their role in the pathogenesis of atherosclerosis, plaque rupture and thrombosis, medial ischemia leading to arterial dissection and aneurysm, restenosis after angioplasty, and post-stenotic dilatation. Finally, larger veins also have an extensive network of vasa that have been implicated in the pathogenesis of venous thrombosis and varicose veins.