Hemodynamics and low density lipoprotein metabolism. Rates of low density lipoprotein incorporation and degradation along medial and lateral walls of the rabbit aorto-iliac bifurcation.
Hemodynamics and low density lipoprotein metabolism. Rates of low density lipoprotein incorporation and degradation along medial and lateral walls of the rabbit aorto-iliac bifurcation.
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DOI：
10.1161/01.atv.10.5.686
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发表时间：
1990-09
期刊：
影响因子：
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通讯作者：
S. Berceli;V. Warty;R. Sheppeck;W. A. Mandarino;S K Tanksale;H. Borovetz
中科院分区：
文献类型：
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作者：
S. Berceli;V. Warty;R. Sheppeck;W. A. Mandarino;S K Tanksale;H. Borovetz
我们已经调查了是否动脉壁低密度脂蛋白（LDL）的代谢在干扰流的地区不同于在邻近地区的未受干扰流的代谢。以兔主动脉-髂动脉分叉为模型，我们检查了体内低密度脂蛋白掺入率和分解代谢率，并将其与这些区域的动脉血流模式相关。采用捕获配体法定量测定子髂分支的三个血流动力学区域在20小时内的LDL掺入率和降解率：1）流动分离区域，其中剪切力沿内侧壁沿着升高，沿外侧壁沿着降低，2）过渡区域，其中流型开始接近完全建立的情况，和3）单向流动区域，其具有沿中间壁和侧壁沿着对称的流体剪切力。我们的研究结果表明，在血流分离的近端区域，LDL掺入外侧壁与内侧壁的速率升高（5.2 +/- 0.8 nl/mg/hr vs. 3.7 +/- 0.5 nl/mg/hr，p <0.01）。还观察到该最近端区域外侧壁的降解速率高于内侧壁（2.1 +/- 0.4 vs. 1.4 +/- 0.2，p <0.05）。在过渡或单向血流动力学区域中，未观察到LDL掺入和降解的此类差异。这些结果表明，动脉壁LDL掺入和catalysts的修改是由血液动力学的力量。这些发现的影响，动脉粥样硬化病变的形成进行了讨论。
We have investigated whether arterial wall low density lipoprotein (LDL) metabolism in areas of disturbed flow differs from the metabolism in adjacent regions of undisturbed flow. Using the rabbit aorto-iliac bifurcation as a model, we examined the rates of LDL incorporation and catabolism in vivo and correlated them to the arterial flow patterns in these regions. The trapped ligand method was used to quantitate the rates of LDL incorporation and degradation over a 20-hour period in three hemodynamic zones of the daughter iliac branch: 1) a region of flow separation where the shearing forces are elevated along the medial wall and reduced along the lateral wall, 2) a transition region where the flow patterns begin to approach the fully established situation, and 3) a unidirectional flow region with symmetric fluid shearing forces along the medial and lateral walls. Our results indicate an elevated rate of LDL incorporation into the lateral versus the medial wall in the proximal zone of flow separation (5.2 +/- 0.8 nl/mg/hr vs. 3.7 +/- 0.5 nl/mg/hr, p less than 0.01). A similar elevation in the degradation rate of the lateral over the medial wall of this most proximal zone was also observed (2.1 +/- 0.4 vs. 1.4 +/- 0.2, p less than 0.05). No such differences were observed regarding LDL incorporation and degradation in the transitional or unidirectional hemodynamic zones. These results suggest that modifications in arterial wall LDL incorporation and catabolism are induced by hemodynamic forces. The implications of these findings for the formation of the atherosclerotic lesion are discussed.