Mascelli M A, Worley S, Veriabo N J, Lance E T, Mack S, Schaible T, Weisman H F, Jordan R E
Pharmaceutical Division, Centocor Inc, Malvern, Pa 19355-1307, USA.
Circulation. 1997 Dec 2;96(11):3860-6. doi: 10.1161/01.cir.96.11.3860.
The glycoprotein (GP) IIb/IIIa receptor antagonist abciximab (c7E3 Fab, ReoPro) is approved for use in high-risk percutaneous transluminal coronary angioplasty (PTCA). At present, no "point of care" exists for measuring pharmacological GP IIb/IIIa blockade. To address this need, the Chrono-log Whole Blood Aggregometer, which measures platelet aggregation by electrical impedance, was adapted to test platelet function at the bedside.
GP IIb/IIIa receptor blockade, impedance (5 microg/mL collagen), and turbidimetric aggregation (5 and 20 micromol/L ADP) measurements were obtained on 14 PTCA patients who received the standard bolus plus a 12-hour infusion of abciximab. During abciximab administration, mean GP IIb/IIIa receptor blockade was > 91%, and both impedance and turbidimetric aggregation were inhibited by > or = 90%. At 12 hours after abciximab treatment, the mean inhibition of turbidimetric platelet aggregation to 5 and 20 micromol/L ADP was 65+/-20% and 49+/-14%, respectively, and inhibition of impedance aggregation was 69+/-12%. GP IIb/IIIa receptor blockade was 67+/-8%. At 36 hours after abciximab treatment (n=8), the mean inhibition of turbidimetric platelet aggregation to 5 and 20 micromol/L ADP was 44+/-21% and 30+/-14%, respectively, whereas impedance aggregation was inhibited by 60+/-14%. GP IIb/IIIa receptor blockade was 57+/-7%.
During and at 12 hours after abciximab therapy, impedance and turbidimetric platelet aggregation to 5 micromol/L ADP were comparable and closely correlated with GP IIb/IIIa receptor blockade. However, at 36 hours after abciximab treatment, impedance platelet aggregation more closely paralleled GP IIb/IIIa receptor blockade and indicated a slower recovery of platelet function than turbidimetric aggregometry.
糖蛋白（GP）IIb/IIIa受体拮抗剂阿昔单抗（c7E3 Fab，ReoPro）已被批准用于高危经皮腔内冠状动脉成形术（PTCA）。目前，尚无用于测量GP IIb/IIIa药理学阻断的“床旁检测”方法。为满足这一需求，对通过电阻抗测量血小板聚集的Chrono-log全血凝集仪进行了改进，以在床旁检测血小板功能。
对14例接受标准推注加12小时阿昔单抗输注的PTCA患者进行了GP IIb/IIIa受体阻断、阻抗（5微克/毫升胶原）和比浊法聚集（5和20微摩尔/升ADP）测量。在阿昔单抗给药期间，平均GP IIb/IIIa受体阻断率>91%，阻抗和比浊法聚集均受到>或 = 90%的抑制。阿昔单抗治疗12小时后，比浊法血小板对5和20微摩尔/升ADP聚集的平均抑制率分别为65±20%和49±14%，阻抗聚集的抑制率为69±12%。GP IIb/IIIa受体阻断率为67±8%。阿昔单抗治疗36小时后（n = 8），比浊法血小板对5和20微摩尔/升ADP聚集的平均抑制率分别为44±21%和30±14%，而阻抗聚集的抑制率为60±14%。GP IIb/IIIa受体阻断率为57±7%。
在阿昔单抗治疗期间及治疗后12小时，血小板对5微摩尔/升ADP的阻抗和比浊法聚集具有可比性，且与GP IIb/IIIa受体阻断密切相关。然而，在阿昔单抗治疗36小时后，阻抗血小板聚集与GP IIb/IIIa受体阻断更为平行，表明血小板功能的恢复比比浊法聚集测定法更慢。
