Sloand E M, Alyono D, Klein H G, Chang P, Yu M, Lightfoot F G, Kessler C
Department of Transfusion Medicine, Warren Grant Magnuson Clinical Center, National Institutes of Health, Bethesda, Maryland 20892.
Am J Hematol. 1994 Jul;46(3):199-207. doi: 10.1002/ajh.2830460308.
1-deamino-8-D-Arginine vasopressin (DDAVP) shortens the bleeding time in some patients with platelet dysfunction and decreases blood loss in some cardiopulmonary bypass patients. We studied platelet membrane glycoproteins in patients with von Willebrand disease (vWD), disorders of platelet function, and in cardiopulmonary bypass patients after infusion of 0.3 microgram/kg of DDAVP. Platelets from 8 cardiopulmonary bypass patients, receiving DDAVP immediately after surgery, were compared to those of 14 patients not receiving DDAVP. We also studied 12 patients with vWD, and 8 patients with platelet dysfunction receiving DDAVP. Fixed platelets, stained with monoclonal fluorescein (FITC)-labeled antibodies directed against GPIb (CD42b antigen), GPIb/IX, GPIIb/IIIa (CD41a antigen), CD63 antigen (a platelet activation protein), and P-selectin (CD62 antigen) were studied by flow cytometry. Binding of CD42b monoclonal antibody (MoAb) and anti-GPIb/IX to platelets from both groups of bypass patients increased during the 18-20 hr after surgery, but the group receiving DDAVP showed the greater increase (P = 0.032). Platelets from patients receiving DDAVP for vWD or for platelet dysfunction, had increases in CD42b MoAb and anti-GPIb/IX binding (P < 0.01) that coincided with shortening of their bleeding time. No changes were seen in binding of other antibodies. When platelets from normal donors were incubated with DDAVP for 20 hr, there were increases in platelet surface CD42b MoAb binding, while immunogold-stained transmission electron micrographs of permeabilized platelets demonstrated decreases in cytoplasmic CD42b MoAb binding. DDAVP increases platelet membrane GPIb expression in a variety of patients and may account for improvement in hemostasis seen in some studies. Redistribution of GPIb from the cytoplasm to the membrane may account for this increased expression.
1-去氨基-8-D-精氨酸血管加压素(DDAVP)可缩短某些血小板功能障碍患者的出血时间,并减少某些体外循环患者的失血量。我们研究了血管性血友病(vWD)患者、血小板功能障碍患者以及输注0.3微克/千克DDAVP后的体外循环患者的血小板膜糖蛋白。将8例体外循环术后立即接受DDAVP的患者的血小板与14例未接受DDAVP的患者的血小板进行比较。我们还研究了12例vWD患者和8例接受DDAVP的血小板功能障碍患者。通过流式细胞术研究了用针对糖蛋白Ib(CD42b抗原)、糖蛋白Ib/IX、糖蛋白IIb/IIIa(CD41a抗原)、CD63抗原(一种血小板活化蛋白)和P-选择素(CD62抗原)的单克隆荧光素异硫氰酸酯(FITC)标记抗体染色的固定血小板。两组体外循环患者术后18 - 20小时内,CD42b单克隆抗体(MoAb)和抗糖蛋白Ib/IX与血小板的结合均增加,但接受DDAVP的组增加幅度更大(P = 0.032)。接受DDAVP治疗vWD或血小板功能障碍的患者的血小板,其CD42b MoAb和抗糖蛋白Ib/IX结合增加(P < 0.01),且与出血时间缩短一致。其他抗体的结合未见变化。当正常供体的血小板与DDAVP孵育20小时后,血小板表面CD42b MoAb结合增加,而经透化处理的血小板的免疫金染色透射电子显微镜图像显示细胞质CD42b MoAb结合减少。DDAVP可增加多种患者的血小板膜糖蛋白Ib表达,这可能是一些研究中所见止血改善的原因。糖蛋白Ib从细胞质重新分布到细胞膜可能是这种表达增加的原因。