Baskurt Oguz K
Department of Physiology, Faculty of medicine, Akdeniz University, Antalya, Turkey.
Biorheology. 2008;45(6):629-38.
It is has been known for more than 80 years that compared to in vitro determinations, blood behaves as a less viscous fluid under in vivo flow conditions. The experiments of Whittaker and Winton were among the first dealing with the in vivo effects of altered blood rheology, and experimental studies during the second half of 20th century have provided additional evidence for the complexity of in vivo hemodynamics-hemorheology relationships. Careful studies indicate that the impact of a given blood rheology alteration is determined by the properties of the experimental model (e.g., organ or tissue under investigation), experimental approach (e.g., intravital microscopy, whole organ perfusion) and method used to modify blood rheology. In addition, vascular control mechanisms may play a major role in the resulting hemodynamic effects of a hemorheological alteration: (1) a response simply related to metabolic autoregulation in which there is a compensatory vasodilation due to altered in vivo blood flow and organ/tissue hypoxia; (2) modulation of endothelial function (e.g., NO production) via altering wall shear stress, thereby leading to changes of vascular hindrance. The in vivo effects of altered red blood cell (RBC) aggregation have been investigated in various experimental models. A novel technique for modifying RBC aggregability (i.e., intrinsic tendency of RBC to aggregate) by covalent attachment of specific co-polymers has been used in some studies, and has provided data reflecting the specific effects of RBC aggregation without the influence of altered suspending phase properties. These data indicate that both the magnitude of the hemodynamic effect and the direction of the alteration depend on the intensity of RBC aggregation. Using the same novel technique, RBC aggregation has been shown to be an important determinant of endothelial function through its effects on RBC axial distribution and wall shear stress. These somewhat diverse findings can be explained by considering the contribution of various in vivo hemorheological mechanisms that have opposite effects on in vivo flow resistance.
八十多年来，人们已经知道，与体外测定相比，在体内流动条件下血液表现为粘性较低的流体。惠特克和温顿的实验是最早涉及血液流变学改变的体内效应的实验之一，20世纪后半叶的实验研究为体内血液动力学 - 血液流变学关系的复杂性提供了更多证据。仔细研究表明，给定血液流变学改变的影响取决于实验模型的特性（例如，所研究的器官或组织）、实验方法（例如，活体显微镜检查、全器官灌注）以及用于改变血液流变学的方法。此外，血管控制机制可能在血液流变学改变所产生的血液动力学效应中起主要作用：（1）一种仅与代谢自动调节相关的反应，其中由于体内血流改变和器官/组织缺氧而出现代偿性血管舒张；（2）通过改变壁面切应力来调节内皮功能（例如，一氧化氮生成），从而导致血管阻力的变化。在各种实验模型中研究了红细胞（RBC）聚集改变的体内效应。一些研究中使用了一种通过特定共聚物的共价连接来改变RBC聚集性（即RBC聚集的内在倾向）的新技术，该技术提供了反映RBC聚集的特定效应而不受悬浮相性质改变影响的数据。这些数据表明，血液动力学效应的大小和改变的方向都取决于RBC聚集的强度。使用相同的新技术，RBC聚集已被证明是内皮功能的重要决定因素，通过其对RBC轴向分布和壁面切应力的影响。通过考虑各种对体内流动阻力有相反作用的体内血液流变学机制的贡献，可以解释这些有些不同的发现。
