Aarts P A, Banga J D, van Houwelingen H C, Heethaar R M, Sixma J J
Blood. 1986 May;67(5):1474-81.
Platelet transport towards the vessel wall is influenced by the hematocrit, red blood cell (RBC) size, and shape. Recent in vitro studies have indicated that RBC deformability may also influence platelet transport. The observation that isoxsuprine, a known vasodilating drug, caused increased RBC deformability in vitro and decreased platelet transport in vitro prompted us to study the effects of this drug in vivo. The study was performed in a double-blind cross-over study of isoxsuprine v placebo in ten patients with peripheral arterial insufficiency. RBC deformability was estimated from viscosity measurements using the blood viscosity equation of Dintenfass and expressed as T value. Platelet transport was studied in an annular perfusion chamber according to Baumgartner. Human umbilical arteries were used as blood vessels. Perfusion studies were performed with whole blood or with RBCs of the patients mixed with normal platelets and plasma at a standardized hematocrit and platelet count. An increase in RBC deformability concomitant with a decrease in platelet adherence was observed in patients on isoxsuprine with a drop in T value of approximately 0.06 (from 0.91 toward 0.86), and a concomitant decrease in platelet adherence of 20% to 40%. These observations differed significantly from the results in the placebo group and showed a significant group-period interaction at the cross-over of medication (analysis of variance). The effects on platelet adherence were observed at high vessel wall shear rate (1,800 s-1) with perfusates consisting of patients' RBCs and donor plasma and platelets at standardized hematocrit and platelet count. No differences were observed under these conditions at a shear rate of 300 s-1. When whole blood of patients was used, nonsignificant effect was observed at shear rates of 300 s-1 and 1,800 s-1. This was probably caused by the added noise due to variations in hematocrit and platelet number. These data demonstrate that isoxsuprine increases RBC deformability, and they suggest the possibility of decreasing platelet-vessel wall interaction in vivo by manipulation of RBC deformability.
血小板向血管壁的运输受血细胞比容、红细胞（RBC）大小和形状的影响。最近的体外研究表明，红细胞变形性也可能影响血小板运输。已知血管扩张药物异舒普林在体外可导致红细胞变形性增加且体外血小板运输减少，这一观察结果促使我们研究该药物在体内的作用。本研究在10例外周动脉供血不足患者中进行了异舒普林与安慰剂的双盲交叉研究。根据丁滕法斯血液黏度方程通过黏度测量估计红细胞变形性，并表示为T值。按照鲍姆加特纳法在环形灌注室中研究血小板运输。用人脐动脉作为血管。在标准化血细胞比容和血小板计数条件下，用全血或患者的红细胞与正常血小板及血浆混合进行灌注研究。服用异舒普林的患者中观察到红细胞变形性增加，同时血小板黏附减少，T值下降约0.06（从0.91降至0.86），血小板黏附同时减少20%至40%。这些观察结果与安慰剂组的结果有显著差异，并且在药物交叉时显示出显著的组-时期交互作用（方差分析）。在高血管壁剪切速率（1800 s-1）下，用由患者红细胞、供体血浆和血小板组成的灌注液在标准化血细胞比容和血小板计数条件下观察到对血小板黏附的影响。在这些条件下，剪切速率为300 s-1时未观察到差异。当使用患者的全血时，在剪切速率为300 s-1和1800 s-1时观察到无显著影响。这可能是由于血细胞比容和血小板数量变化导致的额外干扰所致。这些数据表明异舒普林可增加红细胞变形性，并提示通过控制红细胞变形性在体内减少血小板与血管壁相互作用的可能性。
