Stoltz J F, Donner M
U.284 INSERM Université Nancy I, Brabois, Vandoeuvre-les-Nancy, France.
Schweiz Med Wochenschr Suppl. 1991;43:41-9.
It has now been clearly established that blood behaves like a non-Newtonian fluid exhibiting specific features with the probable existence of a plasticity threshold, a viscosity that varies as a function of shear rate and a non-homogeneous nature of the medium during flow. When apparent blood viscosity is represented as a function of shear rate, a high viscosity is observed at low shear rates, mainly due to rouleaux formation or red cell aggregates. At high shear rates, viscosity decreases. Apparent blood viscosity is mainly dependent on the following parameters: cell volume concentration (hematocrit); plasma viscosity (which is itself dependent on the type and concentration of the proteins); mechanical properties of the red cells, the main determinants being the cell membrane and internal viscosity; red blood cell aggregation; shear stress applied. Pathological changes in one of the factors controlling blood viscosity and the resulting clinical symptoms constitute the hyperviscosity syndromes. The field of hyperviscosity syndromes concern the situations where the increased blood viscosity and the accompanying modifications in flow resistance must be considered as being the result of the overall rheological behaviour of blood. In this general context, hyperviscosity syndromes can be divided into 4 main groups: 1. Increase in the number of blood cells (mainly red cells) 2. Increase in the plasma protein concentrations or the appearance of high amounts of a monoclonal protein 3. Increase in internal red cell viscosity or a change in the mechanical properties of the erythrocyte membrane 4. Increase in erythrocyte aggregation (formation of barely or in no way dissociable aggregates). Considered from a hemodynamic viewpoint, the appearance of a hyperviscosity syndrome could (by 'feed back' mechanisms) enhance the phenomenon and slow down blood flow or even stop flow completely, thus making ischemia and thrombosis easier. Further, the appearance of the syndrome also results in a decrease in the blood's overall oxygen transport capacity, which, at a primary approach, is proportional to the ratio hematocrit/blood viscosity.
现已明确证实,血液表现得如同非牛顿流体,具有特定特征,可能存在可塑性阈值、随剪切速率变化的粘度以及流动过程中介质的非均匀性质。当表观血液粘度表示为剪切速率的函数时,在低剪切速率下观察到高粘度,这主要是由于红细胞缗钱状聚集或红细胞聚集体形成。在高剪切速率下,粘度降低。表观血液粘度主要取决于以下参数:细胞体积浓度(血细胞比容);血浆粘度(其本身取决于蛋白质的类型和浓度);红细胞的力学性质,主要决定因素是细胞膜和内部粘度;红细胞聚集;施加的剪切应力。控制血液粘度的因素之一发生病理变化以及由此产生的临床症状构成高粘滞综合征。高粘滞综合征领域涉及这样的情况,即血液粘度增加以及随之而来的流动阻力变化必须被视为血液整体流变行为的结果。在这种一般情况下,高粘滞综合征可分为4个主要组:1. 血细胞数量增加(主要是红细胞);2. 血浆蛋白浓度增加或出现大量单克隆蛋白;3. 红细胞内部粘度增加或红细胞膜力学性质改变;4. 红细胞聚集增加(形成几乎不可解离或完全不可解离的聚集体)。从血液动力学角度考虑,高粘滞综合征的出现可能(通过“反馈”机制)加剧这一现象,减缓血流甚至完全停止血流,从而使缺血和血栓形成更容易发生。此外,该综合征的出现还会导致血液整体氧运输能力下降,初步来看,这与血细胞比容/血液粘度的比值成正比。