RANE Center at St. Dominic's Memorial Hospital, Jackson, Miss.
RANE Center at St. Dominic's Memorial Hospital, Jackson, Miss.
J Vasc Surg Venous Lymphat Disord. 2017 Nov;5(6):864-874. doi: 10.1016/j.jvsv.2017.05.024. Epub 2017 Sep 1.
Peripheral venous hypertension and microvascular injury have merged as central features of chronic venous disease. Peripheral venous pressure in the lower limb is controlled by central and peripheral mechanisms. In the current manuscript, we examine the role of peripheral factors, particularly conduit capacitance compliance, focal stenosis, and arterial inflow into the calf.
An experimental venous model using Penrose tubing as a venous analogue was used where the aforementioned parameters could be manipulated. Volume-pressure curves were derived in the static mode. The dynamic model attempted to simulate key pressure parameters of lower limb venous flow.
Decreasing compliance resulted in progressive reduction of conduit capacitance affecting both bending and stretching regimens and the relative distribution between the two, rotating the volume-pressure curve toward the x-axis. Increased postcapillary (arterial) inflow increased conduit pressure. For a given inflow, pressures varied inversely to conduit caliber. Decreased compliance led to a smaller functional caliber at working pressures. Sideline capacitance with stagnant flow connected to the flow channel (simulating calf vein network) did not influence conduit pressure. Focal stenosis increased "venous pressure" if it was narrower than "optimum outflow caliber," defined as the minimum outflow conduit caliber required to balance inflow. Percentage stenosis as traditionally calculated using adjacent lumen as denominator was uncorrelated to pressure increase.
Conduit pressure is increased with smaller native or functional (poor compliance) caliber, focal stenosis, and increased postcapillary inflow. Many of these features appear to be present in limbs clinically suspected of chronic venous disease. The importance of the geometric factor of Poiseuille equation in pressure effects of caliber reduction and collateralization is discussed.
外周静脉高压和微血管损伤已成为慢性静脉疾病的中心特征。下肢外周静脉压力受中枢和外周机制控制。在本手稿中，我们研究了外周因素的作用，特别是输送管电容顺应性、局灶性狭窄和流入小腿的动脉。
使用彭罗斯管作为静脉类似物的实验静脉模型，可在此模型中操纵上述参数。在静态模式下得出体积-压力曲线。动态模型试图模拟下肢静脉血流的关键压力参数。
顺应性降低导致输送管电容逐渐减少，影响弯曲和拉伸方案以及两者之间的相对分布，使体积-压力曲线向 x 轴旋转。增加毛细血管后（动脉）流入增加输送管压力。对于给定的流入，压力与输送管口径成反比。顺应性降低导致工作压力下的功能口径减小。与流动通道（模拟小腿静脉网络）连接的静止流动的旁通电容不会影响输送管压力。如果狭窄比“最佳流出口径”（定义为平衡流入所需的最小流出输送管口径）更窄，则局灶性狭窄会增加“静脉压力”。传统上使用相邻腔作为分母计算的狭窄百分比与压力增加无关。
输送管压力随着固有或功能（顺应性差）口径减小、局灶性狭窄和毛细血管后流入增加而增加。在临床上怀疑患有慢性静脉疾病的肢体中，这些特征似乎很多都存在。讨论了泊肃叶方程的几何因素在口径减小和侧支形成中的压力效应中的重要性。
