Effects of elastin degradation and surrounding matrix support on artery stability
Effects of elastin degradation and surrounding matrix support on artery stability
复制标题
DOI：
10.1152/ajpheart.00463.2011
复制
发表时间：
2012-02-01
影响因子：
4.8
通讯作者：
Han, Hai-Chao
中科院分区：
文献类型：
--
作者：
Lee, Avione Y.;Han, Boyang;Han, Hai-Chao
Lee AY，Han B，Lamm SD，Fierro CA，Han HC.弹性蛋白降解和周围基质支持对动脉稳定性的影响。Am J Physiol Heart Circ Physiol 302：H873-H884，2012.首次出版于2011年12月9日; doi：10.1152/ajpheart. 00463.2011.-迂曲动脉通常与衰老、高血压、动脉粥样硬化和退行性血管疾病有关，但其机制知之甚少。我们最近的理论分析表明，机械不稳定性（屈曲）可能会导致扭曲的血管。本研究的目的是确定动脉屈曲的临界压力以及弹性蛋白降解和周围基质支持对动脉机械稳定性的影响。采用加压充气和屈曲试验，测定了一组5条正常动脉的力学性能和临界屈曲压力，在临界屈曲压力下，动脉变得不稳定并变形成迂曲形状。另一组9条猪动脉用弹性蛋白酶（8 U/ml）处理，测定处理前后的机械刚度和临界压力。使用明胶凝胶模拟周围组织支持的效果。在轴向拉伸比为1.3和1.5时，5条正常动脉的临界压力分别为9.52 kPa（SD 1.53）和17.10 kPa（SD 5.11），而模型预测的临界压力分别为10.11 kPa（SD 3.12）和17.86 kPa（SD 5.21）。弹性蛋白酶处理显著降低了临界屈曲压力（P < 0.01）。在较高的临界压力下，具有周围基质支撑的动脉屈曲成多个波。我们的结论是，动脉屈曲管腔压力下可以预测的屈曲方程。弹性蛋白降解会削弱动脉壁并降低临界压力，从而导致血管迂曲。这些结果揭示了由于弹性蛋白缺乏而导致的迂曲血管的发展机制。
Lee AY, Han B, Lamm SD, Fierro CA, Han HC. Effects of elastin degradation and surrounding matrix support on artery stability. Am J Physiol Heart Circ Physiol 302: H873-H884, 2012. First published December 9, 2011; doi: 10.1152/ajpheart. 00463.2011.-Tortuous arteries are often associated with aging, hypertension, atherosclerosis, and degenerative vascular diseases, but the mechanisms are poorly understood. Our recent theoretical analysis suggested that mechanical instability (buckling) may lead to tortuous blood vessels. The objectives of this study were to determine the critical pressure of artery buckling and the effects of elastin degradation and surrounding matrix support on the mechanical stability of arteries. The mechanical properties and critical buckling pressures, at which arteries become unstable and deform into tortuous shapes, were determined for a group of five normal arteries using pressurized inflation and buckling tests. Another group of nine porcine arteries were treated with elastase (8 U/ml), and the mechanical stiffness and critical pressure were obtained before and after treatment. The effect of surrounding tissue support was simulated using a gelatin gel. The critical pressures of the five normal arteries were 9.52 kPa (SD 1.53) and 17.10 kPa (SD 5.11) at axial stretch ratios of 1.3 and 1.5, respectively, while model predicted critical pressures were 10.11 kPa (SD 3.12) and 17.86 kPa (SD 5.21), respectively. Elastase treatment significantly reduced the critical buckling pressure (P < 0.01). Arteries with surrounding matrix support buckled into multiple waves at a higher critical pressure. We concluded that artery buckling under luminal pressure can be predicted by a buckling equation. Elastin degradation weakens the arterial wall and reduces the critical pressure, which thus leads to tortuous vessels. These results shed light on the mechanisms of the development of tortuous vessels due to elastin deficiency.