Maurice G, Wang X, Lehalle B, Stoltz J F
Hémorhéologie, Angiohématologie, Equipe LEMTA UMR CNRS 7563, Faculté de Médecine, Vandoeuvre les Nancy.
J Mal Vasc. 1998 Oct;23(4):282-8.
As in most living tissues, a network of nutritional vessels, the so-called vasa vasorum, irrigates the vessel wall under physiological conditions. An alteration or obstruction of this network can induce severe lesions. Most normal arteries and veins are irrigated by a vasa vasorum network located mainly in the adventice. They essentially supply oxygen to the outer layers of the vascular wall, the inner layer being mainly oxygenated by direct diffusion from bloodstream. Vasa vasorum responds to vasomotor stimuli and can even regress, e.g., after vascularization of arterial grafts. Their pathophysiological importance for arteries is now established. Indeed, it is known that an infusion disorder or vasa vasorum alteration may induce or promote early atherosclerotic lesions, fibrodysplasia or even media necrosis. From a mechanical point of view, and considering the three layers as a unique material, the vessel shows non-isotropic linear elastic and incompressible (v = 0.5) behaviour in the case of minimal or moderate deformation. But in the case of major deformation, the vessel displays a non-linear behaviour. The interaction between vasa vasorum supply and the mechanical properties of the arterial vascular wall can promote the occurrence of aneurysms as soon as vasa vasorum irrigation decreases. Some authors have hypothesized that these microvessels could fulfil the same function in the venous wall. It appears also that microcirculation flow rates are lower in varicose veins than in healthy ones and that partial oxygen pressure, already low in a healthy vein media, is even lower in a varicose vein. All these facts underline the importance of supply by the vasa vasorum network and its determining role in maintaining vascular wall integrity. In addition, the influence of vessel non-linear properties and their pathological changes on microcirculation would partially explain media necrosis in arteries and veins. Studying vascular wall deformation under the influence of intraluminal pressure revealed that an initially circular vasa vasorum rapidly takes on an elliptical shape which results more from crosswise circumferential stretching of the wall than from radial crushing. This induces increased hydraulic resistance. Thus permanent overpressure reduces vascular wall irrigation. Once the wall has been devascularized, it will loose its elasticity, harden and retain its maximal deformation. A vicious circle is then created. This phenomenon, noticeable in arteries, could be more serious in veins because their walls are thinner and elasticity modulus is lower. For example, for an intraluminal overpressure of 100 mmHg in an artery and 10 mmHg in a vein the ellipticity of the vasa vasorum becomes 1.2 and 3 respectively. Based on the hypothesis of a linear elastic behaviour and a periodical intraluminal overpressure, the ratio of the two axis of an arterial vasa vasorum B/A varies from 1.13 to 1.28 for Pa = 100 + 30 sin (2 pi t) mmHg, and from 1.24 to 1.44 for Pa = 160 + 40 sin (2 pi t) mmHg. In this case, the ratio of hydraulic resistances R(ellipse)/R(circle) changes little (less than 1, the ratio of the axis varies from 1.1 to 2.6 for Pa = 5 + 5 sin (2 pi t) mmHg) and from 1.8 to 5.8 for Pa = 10 + 5 sin (2 pi t) mmHg). Thus the ratio of hydraulic resistance varies from 1 to 1.5 and from 1.2 to 2.8 respectively. In practice Young's modulus increases in parallel with luminal pressure by limiting vascular wall and vasa vasorum deformation. If we consider the non-linear behaviour of the vessel wall and suppose the same conditions of intraluminal pressure, the ratio of the axis of the venous vasa vasorum in a hypertensive patient varies from 1.6 to 2.6 (instead of 1.8 to 5.8 in the case of linear model). This ratio is higher than that of the healthy subject which is less than 1.7. So the vascular structure in physiological conditions itself reacts to the pressure increases which may jeopardize vasa vasorum irrigation by delaying mural transfor
与大多数活组织一样，在生理条件下，一个营养血管网络，即所谓的血管滋养管，为血管壁供血。该网络的改变或阻塞可引发严重病变。大多数正常动脉和静脉由主要位于外膜的血管滋养管网络供血。它们主要为血管壁的外层提供氧气，内层主要通过从血流中直接扩散来进行氧合。血管滋养管对血管舒缩刺激有反应，甚至会退化，例如在动脉移植物血管化后。其对动脉的病理生理重要性现已明确。确实，已知灌注紊乱或血管滋养管改变可能诱发或促进早期动脉粥样硬化病变、纤维发育异常甚至中层坏死。从力学角度来看，将三层视为一种独特材料，在最小或中等变形情况下，血管表现出非各向同性的线性弹性和不可压缩（泊松比(v = 0.5)）行为。但在大变形情况下，血管表现出非线性行为。一旦血管滋养管灌注减少，血管滋养管供血与动脉血管壁力学性能之间的相互作用就会促使动脉瘤的发生。一些作者推测这些微血管在静脉壁中可能发挥相同功能。似乎静脉曲张中的微循环流速也低于健康静脉，而且健康静脉中层已经较低的局部氧分压在静脉曲张中甚至更低。所有这些事实都强调了血管滋养管网络供血的重要性及其在维持血管壁完整性方面的决定性作用。此外，血管非线性特性及其病理变化对微循环的影响将部分解释动脉和静脉中的中层坏死。研究管腔内压力影响下的血管壁变形发现，最初呈圆形的血管滋养管会迅速变成椭圆形，这更多是由于血管壁横向周向拉伸而非径向挤压所致。这会导致水力阻力增加。因此，持续的过压会减少血管壁灌注。一旦血管壁缺血，它将失去弹性、变硬并保持其最大变形。然后就会形成恶性循环。这种现象在动脉中较为明显，在静脉中可能更严重，因为静脉壁更薄且弹性模量更低。例如，对于动脉管腔内(100 mmHg)的过压和静脉内(10 mmHg)的过压，血管滋养管的椭圆率分别变为(1.2)和(3)。基于线性弹性行为和周期性管腔内过压的假设，对于(Pa = 100 + 30\sin(2\pi t) mmHg)，动脉血管滋养管的两轴之比(B/A)在(1.13)至(1.
