Microvascular blood viscosity in vivo and the endothelial surface layer
Microvascular blood viscosity in vivo and the endothelial surface layer
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DOI：
10.1152/ajpheart.00297.2005
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发表时间：
2005-12-01
影响因子：
4.8
通讯作者：
Secomb, TW
中科院分区：
文献类型：
--
作者：
Pries, AR;Secomb, TW
体内微血管血液粘度与内皮表层有关。美国生理学杂志心脏循环生理学289：H2657-H2664，2005年。首次发表于2005年7月22日; doi：10.1152/ajpheart. 00297.2005. - 玻璃管中血液的表观粘度随着直径的减小而降低（Fahraeus-Lindqvist效应），并在6-7 μ m处显示出明显的最小值。然而，小血管中的体内流动阻力显著高于体外粘度数据所预测的。厚的内皮表面层（ESL）的存在被认为是这种差异的主要原因。在这里，提出了一个物理模型的微血管流动阻力作为血管直径和红细胞压积在体内的函数，它结合了在体外血液粘度与直径依赖性ESL的影响。该模型的基础上开发的三个微血管网络中观察到的流动分布在大鼠肠系膜392，546，和383血管段，血管直径，网络结构，流速和血细胞比容测定活体显微镜。使用先前描述的血液动力学模拟来预测来自有效血液粘度的假设模型的流量和血细胞比容的分布。ESL厚度对血管直径的依赖性通过最小化速度、流动方向和血细胞比容的预测值与测量数据的偏差来估计。对于直径为10- 40 μ m的血管，层厚度为0.8-1 μ m时获得了最佳结果，对于较小直径的血管，层厚度强烈下降，对于直径为10 μ m的血管，对流动阻力的额外血细胞比容依赖性影响最大。这些结果表明，在体内的流动阻力可以解释在体外血液粘度和ESL的存在，并表示在微血管中的ESL的流变学有效厚度。
Microvascular blood viscosity in vivo and the endothelial surface layer. Am J Physiol Heart Circ Physiol 289: H2657-H2664, 2005. First published July 22, 2005; doi:10.1152/ajpheart. 00297.2005. -The apparent viscosity of blood in glass tubes declines with decreasing diameter (Fahraeus-Lindqvist effect) and exhibits a distinctive minimum at 6-7 mu m. However, flow resistance in vivo in small vessels is substantially higher than predicted by in vitro viscosity data. The presence of a thick endothelial surface layer (ESL) has been proposed as the primary cause for this discrepancy. Here, a physical model is proposed for microvascular flow resistance as a function of vessel diameter and hematocrit in vivo; it combines in vitro blood viscosity with effects of a diameter-dependent ESL. The model was developed on the basis of flow distributions observed in three microvascular networks in the rat mesentery with 392, 546, and 383 vessel segments, for which vessel diameters, network architecture, flow velocity, and hematocrit were determined by intravital microscopy. A previously described hemodynamic simulation was used to predict the distributions of flow and hematocrit from the assumed model for effective blood viscosity. The dependence of ESL thickness on vessel diameter was estimated by minimizing deviations of predicted values for velocities, flow directions, and hematocrits from measured data. Optimal results were obtained with a layer thickness of similar to 0.8-1 mu m for 10- to 40-mu m-diameter vessels and declined strongly for smaller diameters, with an additional hematocrit-dependent impact on flow resistance exhibiting a maximum for similar to 10-mu m-diameter vessels. These results show that flow resistance in vivo can be explained by in vitro blood viscosity and the presence of an ESL and indicate the rheologically effective thickness of the ESL in microvessels.