Price R J, Skalak T C
Department of Biomedical Engineering, University of Virginia, Charlottesville 22908.
Microvasc Res. 1994 Mar;47(2):188-202. doi: 10.1006/mvre.1994.1015.
Hypertension results in structural rarefaction of the microvascular arteriolar network while, conversely, decreasing pressure results in arteriolar proliferation. A remodeling mechanism capable of unifying these results remains elusive. A network model of a transverse arteriole tree was used to test whether adaptations to changes in mean circumferential wall stress (sigma theta) could produce realistic structural remodeling. Vessel diameters and network boundary pressures were assigned using experimental data, and control flows (Qij) and sigma theta ij for each vessel were calculated. Mean sigma theta ij in A2 (Strahler order) vessels (sigma m) was 6.62 x 10(4) dynes/cm2. Input pressure was increased by 35% in simulated one-kidney, one-clip (s1K1C) hypertension or decreased by 30% in simulated main feeder ligation (sMFL). Vessel diameters were adjusted iteratively until each Qij was restored, simulating autoregulation. Wall stresses decreased 15.9% for hypertension (sigma m = 5.57 x 10(4) dynes/cm2), but were elevated 60.9% for main feeder ligation (sigma m = 10.65 x 10(4) dynes/cm2), A stress-growth principle was applied, so that stresses above an upper threshold cause growth while stresses below a lower threshold cause resorption. Individual vessels with sigma theta ij < 5.24 x 10(4) dynes/cm2 were removed while new A2 segments were added to A2 vessels with sigma theta ij > 8.27 x 10(4) dynes/cm2. The network structure was adjusted until all sigma theta ij were within these stress thresholds. The number of A2s decreased 22% in s1K1C and increased 96% in sMFL in quantitative agreement with experimental data, consistent with the hypothesis that wall stress may be an important determinant of network remodeling. Arteriolar proliferation and rarefaction represent adaptations to different hemodynamic conditions, but may be governed by a common stress-growth principle.
高血压会导致微血管小动脉网络的结构稀疏，相反，压力降低则会导致小动脉增生。一种能够统一这些结果的重塑机制仍然难以捉摸。使用横向小动脉树的网络模型来测试对平均周向壁应力（σθ）变化的适应性是否能产生现实的结构重塑。利用实验数据确定血管直径和网络边界压力，并计算每个血管的控制流量（Qij）和σθij。A2（斯特拉勒序）血管中的平均σθij（σm）为6.62×10⁴达因/平方厘米。在模拟的单肾单夹（s1K1C）高血压中，输入压力增加35%，或在模拟的主供血动脉结扎（sMFL）中降低30%。反复调整血管直径，直到每个Qij恢复，模拟自动调节。高血压时壁应力降低15.9%（σm = 5.57×10⁴达因/平方厘米），但主供血动脉结扎时壁应力升高60.9%（σm = 10.65×10⁴达因/平方厘米）。应用应力生长原理，使得高于上限阈值的应力会导致生长，而低于下限阈值的应力会导致吸收。去除σθij < 5.24×10⁴达因/平方厘米的单个血管，同时在σθij > 8.27×10⁴达因/平方厘米的A2血管中添加新的A2节段。调整网络结构，直到所有σθij都在这些应力阈值范围内。s1K1C中A2的数量减少了22%，sMFL中增加了96%，与实验数据在数量上一致，这与壁应力可能是网络重塑的重要决定因素这一假设相符。小动脉增生和稀疏代表了对不同血流动力学条件的适应性变化，但可能受共同的应力生长原理支配。
