van der Kamp K W, van Oeveren W
Thorax Center/Biomedical Technology Center, University Hospital Groningen, The Netherlands.
Int J Artif Organs. 1993 Dec;16(12):836-42.
Heparin coating of an extracorporeal device may reduce blood activation. To evaluate protein and platelet interaction with Duraflo II surface treatment of the cardiopulmonary bypass (CPB) circuit, thirty coronary artery bypass grafting patients were randomly divided into two groups (Duraflo II, n = 15 or Control, n = 15). Binding of antibodies against factor XII, antithrombin III (ATIII) and platelet receptor GpIb were significantly higher (p < 0.01) on the Duraflo II treated surface. Hageman Factor fragment (HFf or factor XIIf) activity observed in the fluid phase tended to be lower in the treated circuits, although complexes of factor XIIf-C1 inhibitor (C1INH) increased by the same extent in both groups. Thrombin was effectively bound on the Duraflo II surface while thrombin-antithrombin III formation was reduced during the first phase of CPB. As expected, this thrombin inhibiting capacity remained higher on the Duraflo II, although in the arterial line a reduction of 10% per hour was observed. This indicated loss of functional bound heparin of the Duraflo II surface. During the second phase of CPB, after release of the aortic crossclamp, factor XII and thrombin were strongly activated in both groups indicated by a sharp increase in concentrations of T/AT complex as well as FPA. Platelet numbers tended to increase more in the control group during CPB than in the Duraflo II group, likely by interaction of platelet GpIb receptors on the Duraflo II treated surface (p < 0.01). However, platelet activation assessed by beta-TG was similar in both groups of patients.(ABSTRACT TRUNCATED AT 250 WORDS)
体外装置的肝素涂层可能会减少血液激活。为评估蛋白质和血小板与心肺旁路(CPB)回路的Duraflo II表面处理之间的相互作用,30例冠状动脉旁路移植术患者被随机分为两组(Duraflo II组,n = 15;对照组,n = 15)。在Duraflo II处理过的表面上,针对因子XII、抗凝血酶III(ATIII)和血小板受体GpIb的抗体结合显著更高(p < 0.01)。在处理过的回路中,液相中观察到的Hageman因子片段(HFf或因子XIIf)活性往往较低,尽管两组中因子XIIf-C1抑制剂(C1INH)复合物的增加幅度相同。凝血酶有效地结合在Duraflo II表面,而在CPB的第一阶段,凝血酶 - 抗凝血酶III的形成减少。正如预期的那样,Duraflo II表面的这种凝血酶抑制能力仍然较高,尽管在动脉管路中每小时观察到10%的下降。这表明Duraflo II表面功能性结合肝素的丧失。在CPB的第二阶段,松开主动脉交叉夹后,两组中的因子XII和凝血酶均被强烈激活,这表现为T/AT复合物以及FPA浓度的急剧增加。在CPB期间,对照组中的血小板数量往往比Duraflo II组增加得更多,这可能是由于血小板GpIb受体与Duraflo II处理过的表面相互作用所致(p < 0.01)。然而,通过β - TG评估的血小板激活在两组患者中相似。(摘要截断于250字)