Williams J K, Heistad D D
Comparative Medicine Clinical Research Center, Bowman Gray School of Medicine, Winston-Salem, North Carolina 27175-1040, USA.
J Mal Vasc. 1996;21 Suppl C:266-9.
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.
动脉的营养供应是通过从血管腔以及从滋养血管进行扩散来实现的。大多数正常动脉在外膜中有广泛的滋养血管网络，这些滋养血管起源于母动脉的分支点。当动脉厚度超过营养物质从管腔简单扩散的能力时（如较大的肌性动脉或动脉粥样硬化动脉），滋养血管会延伸至中膜和内膜。内膜 - 中膜的滋养血管主要起源于外膜滋养血管，但在血管移植物以及血栓形成后再通的动脉中，也可起源于管腔。滋养血管对血管活性刺激有反应，并且在使动脉移植物血管化后以及对动脉粥样硬化病变消退时会退化。因此，滋养血管可通过扩张现有动脉或形成新血管（新生血管形成）来增加流向动脉壁的血流量。相反，滋养血管可通过主动收缩或现有滋养血管的退化（ involution ）来减少流向动脉壁的血流量。正常和病变动脉中滋养血管的病理生理意义与其结构有关。内膜 - 中膜的滋养血管是薄壁的内皮细胞管，中膜平滑肌细胞薄或缺失。因此，它们容易因动脉压力、动脉中的机械力、病变动脉中发现的坏死物质以及血管痉挛而塌陷和破裂。滋养血管还为动脉提供了广阔的有吸收功能的内皮表面，这可能对动脉脂质动力学以及神经体液因子从动脉壁的递送和清除具有重要意义。这些特性引发了关于它们在动脉粥样硬化、斑块破裂和血栓形成、导致动脉夹层和动脉瘤的中膜缺血、血管成形术后再狭窄以及狭窄后扩张的发病机制中作用的推测。最后，较大的静脉也有广泛的滋养血管网络，这些滋养血管与静脉血栓形成和静脉曲张的发病机制有关。
