Department of Mechanical Engineering, Biomedical Engineering Program, University of Texas at San Antonio and the University of Texas Health Science Center at San Antonio, San Antonio, TX 78249, USA.
Am J Physiol Heart Circ Physiol. 2012 Feb 15;302(4):H873-84. doi: 10.1152/ajpheart.00463.2011. Epub 2011 Dec 9.
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.
迂曲的动脉通常与衰老、高血压、动脉粥样硬化和退行性血管疾病有关，但机制尚不清楚。我们最近的理论分析表明，机械不稳定性（屈曲）可能导致迂曲的血管。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力学稳定性的影响。使用加压膨胀和屈曲试验，对五组正常动脉确定了其机械性能和临界屈曲压力，即在这些压力下，动脉变得不稳定并变形为迂曲形状。另外九组猪动脉用弹性蛋白酶（8U/ml）处理，在处理前后获得了机械刚度和临界压力。使用明胶凝胶模拟周围组织的支持。五组正常动脉在轴向拉伸比为 1.3 和 1.5 时的临界压力分别为 9.52kPa（SD1.53）和 17.10kPa（SD5.11），而模型预测的临界压力分别为 10.11kPa（SD3.12）和 17.86kPa（SD5.21）。弹性蛋白酶处理显著降低了临界屈曲压力（P<0.01）。有周围基质支持的动脉在较高的临界压力下会屈曲成多个波。我们得出结论，腔内压力下的动脉屈曲可以通过屈曲方程来预测。弹性蛋白降解削弱了动脉壁并降低了临界压力，从而导致迂曲的血管。这些结果阐明了由于弹性蛋白缺乏导致迂曲血管形成的机制。
