Brittain H A, Eckman J R, Wick T M
School of Chemical Engineering, Georgia Institute of Technology, Atlanta 30332-0100.
J Lab Clin Med. 1992 Oct;120(4):538-45.
Complications in sickle syndromes are thought to result from regional disturbances of normal blood flow with subsequent ischemic damage. Adherence of sickle erythrocytes has been implicated in the pathophysiology of occlusive complications. Most previous studies have explored adherence of sickle erythrocytes to endothelial cells from large vessels, even though the majority of the pathophysiologic models implicate the microvascular system. To explore potential variation in endothelial interactions at low shear rates, adherence of sickle erythrocytes to large vessel umbilical vein endothelium and microvascular endothelium was compared under flow conditions in a parallel-plate flow chamber at a shear stress of 1.0 dyne/cm2. Autologous plasma promotes high levels of sickle red cell adherence to microvascular endothelial cells, but only low levels of adherence to human umbilical vein endothelium. On average, autologous plasma promotes sixfold more sickle cell red adherence to microvascular endothelial cells. In contrast to umbilical vein endothelium, high molecular von Willebrand factor does not elevate sickle cell adherence to microvascular endothelial cells, and the integrin receptor agonist peptide, RGD, does not inhibit adherence to microvascular endothelial cells. These results demonstrate that sickle erythrocyte adherence to large vessel and microvascular endothelium is quantitatively and qualitatively different and that plasma factors may have significant impact on sickle erythrocyte adherence to endothelium in the microvessels. Since microvascular occlusion has been suggested as an antecedent of ischemic damage in sickle syndromes, plasma enhanced adherence to microvascular endothelium may contribute to the pathophysiology of episodic occlusion in sickle cell anemia.
镰状细胞综合征的并发症被认为是由正常血流的局部紊乱及随后的缺血性损伤所致。镰状红细胞的黏附被认为与闭塞性并发症的病理生理学有关。尽管大多数病理生理模型涉及微血管系统，但之前的大多数研究都探讨了镰状红细胞与大血管内皮细胞的黏附。为了探究低剪切速率下内皮细胞相互作用的潜在差异，在平行板流动腔中，于1.0达因/平方厘米的剪切应力流动条件下，比较了镰状红细胞与大血管脐静脉内皮细胞和微血管内皮细胞的黏附情况。自体血浆可促进镰状红细胞与微血管内皮细胞的高水平黏附，但与人类脐静脉内皮细胞的黏附水平较低。平均而言，自体血浆促进镰状红细胞与微血管内皮细胞的黏附是其与脐静脉内皮细胞黏附的六倍。与脐静脉内皮细胞不同，高分子量血管性血友病因子不会提高镰状红细胞与微血管内皮细胞的黏附，整合素受体激动剂肽RGD也不会抑制其与微血管内皮细胞的黏附。这些结果表明，镰状红细胞与大血管和微血管内皮细胞的黏附在数量和质量上均存在差异，血浆因子可能对镰状红细胞在微血管中与内皮细胞的黏附产生重大影响。由于微血管闭塞被认为是镰状细胞综合征缺血性损伤的先兆，血浆增强的与微血管内皮细胞的黏附可能有助于镰状细胞贫血发作性闭塞的病理生理过程。
