Berger S A, King W S
Blood Cells. 1982;8(1):153-61.
A model has been developed which couples the transport of oxygen in the capillaries to the motion of sickle cells. A Krogh model is used to model the oxygen transport, while the motion of the HbSS red cells is assumed to be determined by lubrication theory. Reversibly sickled cells are considered, with an assumed dependence of their compliance, or deformability, on the PO2 level. The model predicts that when the pressure gradient driving the cells in the capillary has normal values the cells move faster than normal cells and exit the capillary at relatively high PO2 levels, higher than for normal cells under the same conditions. This is due primarily to the much lower hematocrit typical of sickle-cell disease. Under conditions of reduced driving pressure gradient the situation changes, the cell velocity falls proportionally by an even greater amount, as do the PO2 levels, conditions conducive to the development of the deleterious effects associated with sickling. These results suggest that whereas the compensatory mechanisms in sickle-cell disease are adequate under normal conditions, they may fail under conditions which reduce the pressure gradient across the capillaries, such as vasoconstriction of the arterioles.
已经开发出一种模型,该模型将毛细血管中的氧气运输与镰状细胞的运动耦合起来。使用克勒格模型来模拟氧气运输,而假设HbSS红细胞的运动由润滑理论决定。考虑了可逆镰状化的细胞,并假设它们的顺应性或可变形性取决于PO2水平。该模型预测,当驱动毛细血管中细胞的压力梯度为正常值时,细胞移动速度比正常细胞快,并在相对较高的PO2水平下离开毛细血管,该水平高于相同条件下正常细胞的水平。这主要是由于镰状细胞病典型的血细胞比容低得多。在驱动压力梯度降低的情况下,情况会发生变化,细胞速度按比例下降得更多,PO2水平也是如此,这些条件有利于与镰状化相关的有害影响的发展。这些结果表明,虽然镰状细胞病的代偿机制在正常情况下是足够的,但在降低毛细血管跨壁压力梯度的情况下可能会失效,例如小动脉的血管收缩。