Gu Y J, Boonstra P W, Rijnsburger A A, Haan J, van Oeveren W
Department of Cardiothoracic Surgery, Thorax Center, University Hospital Groningen, The Netherlands.
Ann Thorac Surg. 1998 May;65(5):1342-7. doi: 10.1016/s0003-4975(98)00223-9.
The cardiopulmonary bypass (CPB) circuit induces blood activation and a systemic inflammatory response in cardiac surgical patients. The CPB circuit treated with surface-modifying additive (SMA) has been found to reduce blood activation by in vitro and ex vivo experiments. This study evaluates the surface thrombogenicity and complement activation of SMA circuits during clinical CPB.
Twenty patients undergoing coronary artery bypass grafting were randomly divided into two groups. In the SMA group (n = 10), all blood-contacting surfaces in the CPB circuit were treated or coated with SMA, whereas in the control group (n = 10) patients were perfused with an identical circuit without treatment.
During CPB, platelet count and beta-thromboglobulin were found similar in both the SMA and the control groups. Prothrombin activation indicated by fragment F1 + 2 was found less in the SMA group (p < 0.05). After CPB, platelet deposition on the CPB circuit was significantly less (p < 0.05) in the SMA group than in the control group as assessed by the labeled monoclonal antibody against platelet glycoprotein IIIa. Complement activation identified by C3a and terminal complex C5b-9 did not differ between the two groups, but C4a generation was less in the SMA group (p < 0.05). Leukocyte activation identified by elastase and cytokine release indicated by interleukin-8 were found uniformly in both groups. Postoperatively, chest tube drainage, blood transfusion, duration of ventilatory support, as well as the intensive care unit and hospital stay were not significantly different between the two groups.
These preliminary clinical results suggest that SMA inhibits platelet interaction with the biomaterial surface of the CPB circuit. Complement activation assessed by the terminal complement complex is not influenced by SMA. The clinical benefit of this surface-modifying technique has yet to be assessed in a larger population of patients undergoing cardiac operations.
体外循环（CPB）回路可引发心脏手术患者的血液活化及全身炎症反应。体外和离体实验发现，经表面改性添加剂（SMA）处理的CPB回路可减少血液活化。本研究评估临床CPB期间SMA回路的表面血栓形成性和补体激活情况。
20例行冠状动脉旁路移植术的患者被随机分为两组。在SMA组（n = 10）中，CPB回路中所有与血液接触的表面均用SMA处理或涂层，而在对照组（n = 10）中，患者使用未经处理的相同回路进行灌注。
CPB期间，SMA组和对照组的血小板计数及β-血小板球蛋白水平相似。SMA组中由片段F1 + 2表示的凝血酶原激活较少（p < 0.05）。CPB后，通过抗血小板糖蛋白IIIa标记单克隆抗体评估，SMA组CPB回路上的血小板沉积明显少于对照组（p < 0.05）。通过C3a和末端复合物C5b - 9鉴定的补体激活在两组之间无差异，但SMA组中C4a的生成较少（p < 0.05）。两组中均发现由弹性蛋白酶鉴定的白细胞活化以及由白细胞介素-8表示的细胞因子释放情况相同。术后，两组的胸管引流量、输血量、通气支持时间以及重症监护病房停留时间和住院时间均无显著差异。
这些初步临床结果表明，SMA可抑制血小板与CPB回路生物材料表面的相互作用。通过末端补体复合物评估的补体激活不受SMA影响。这种表面改性技术的临床益处尚未在更多接受心脏手术的患者中进行评估。
