中文摘要：

目的探讨体外循环（CPB）时血小板（PL）的构象与功能变化以及血液麻醉对PL的保护作用。方法人工血管材料聚对苯二甲酸乙二醇脂（polyethylene terephthalate，PET）表面处理后接枝牛血清白蛋白（BSA）成为PET-BSA。取PET和PET—BSA试片进行对比实验：（1）通过PL乳酸脱氢酶（LDH）的定量测定，计算材料表面吸附的PL量；（2）通过PL的膜糖蛋白GMP140单克隆抗体免疫学测定，计算材料表面活化的PL量；（3）在材料表面进行PL吸附实验，通过扫描电镜观察PL的形态。（4）选择体外循环心内直视手术30例随机分为抑肽酶组和对照组；检测转流中不同时期血液中FDP、PK、PLG和TXB，的量；记录24h纵隔和心包引流量；电镜观察PL构象。结果PET-BSA表面吸附的PL量明显低于对照组（P〈0．05），活化PL量仅为对照组的20％。扫描电镜显示白蛋白涂层吸附PL少；对照组PL呈重叠状且有伪足。血液麻醉组较对照组纤维蛋白溶解酶原（PLG）分解少，纤溶系统被抑制，PL结构被保护。结论CPB时血浆蛋白彼此竞争吸附于血管壁上，然后PL与被吸附的血浆蛋白相互作用，PL与构象变化的纤维蛋白在其γ链C端结合位点上结合；同时PL被激活并暴露其GPⅡb/Ⅲa作用位点；构象变化的PL引发凝血的综合进展。抑肽酶的血液麻醉作用是对纤溶酶和激肽释放酶活化的抑制；保护PL结构中的GPⅡb免受破坏，保护了PL术后的凝血功能。

英文摘要：

Objective To study the construction and function of platelet（PL） and the protection of PL by blood anesthesia during the cardiopulmonary bypass （ CPB ）. Methods Bovine serum albumin （ BSA ） was immobilized on the surface of polyethylene terephthalate（PET） which was used as artificial vascular materials,to obtain the samples of PET-BSA. （ 1 ） The quantity of PL adhesion of PET and PET-BSA samples were investigated by lactate dehydrogenase（LDH） test. （2）The quantity of PL activation was investigated by α-granule membrane protein-140 （GMP140） test. （3）PL adhesion test was conducted on the surface of the samples and the morphology of the adhered PL was examined by scanning electron microscopy （SEM）. （4）30 patients undergoing cardiac surgery under CPB were randomly divided into aprotinin group and control group, quantities of FDP, PK, PLG and thromboxance B2 （TXB2 ） in the blood were measured in various time, PLs were observed by electron microscopy, and postoperative blood loss from chest and medium were recorded during first 24 hours. Results Compared with the control group, the quantity of PL adhesion on the PET-BSA samples significantly decreased and the quantity of PL activation of the PET-BSA group was only 20% of the control group. The results of SEM showed PL on PET-BSA surface was few,whereas on the PET surface overlaped and had pseudopodium. The decomposition of PLG is fewer in blood anaesthesia group, indicated the fibrinolytic system was inhibited and construction of PL was protected. Conclusion During CPB, plasma proteins compete against each other to adhere on the tube of CPB ,then PL interact to the adhered proteins, and PL combine with conformation changed fibrin at its C extreme of γ chain. At the same time,PL is activated and its GPⅡb/Ⅲa point is exposed. The function of blood anesthesia of aprotinin is to inhibit the activation of PLG and PK,protect the GPⅡb of PL from being destroyed, and protect the coagulation funcion of PL of postoperation.