Carr Marcus E, Carr Sheryl L, Roa Veronica, McCardell Kathleen A, Greilich Philip E
Department of Internal Medicine, Medical College of Virginia, Virginia Commonwealth University, Richmond, 23298, USA.
Thromb Res. 2002 Nov 1;108(2-3):161-8. doi: 10.1016/s0049-3848(02)00403-6.
Aprotinin interferes with heparin binding to platelets and decreases blood loss during cardiopulmonary bypass (CPB). Heparin abolishes platelet force during CPB, and the extent of platelet force recovery after protamine administration appears to correlate with blood loss. This study assessed the effect of aprotinin on heparin suppression of platelet force.
Platelet force was measured using the Hemodyne Hemostasis Analyzer. Clots were formed from platelet-rich plasma (PRP) by the addition of batroxobin and 10 mM CaCl(2). Clotting conditions included pH 7.4, ionic strength 0.15 M, fibrinogen level 1 mg/ml and 75,000 platelets/microl.
After 1200 s of clotting, force was reduced from 7110+/-1190 to 450+/-450 dyn by 0.2 U/ml of heparin. Platelet force in aprotinin [20 microg/ml (140 KIU/ml)] containing PRP was not suppressed by heparin addition (7480+/-2410 dyn). Aprotinin [40 microg/ml (280 KIU/ml)] addition to previously heparinized plasma counteracted heparin force suppression. Aprotinin (40 microg/ml) increased platelet force from 5630 to 11,138+/-562 in PRP devoid of heparin. Aprotinin did not affect thrombin activity, fibrin structure, platelet aggregation or secretion.
Aprotinin counteracts heparin suppression of platelet force and enhances platelet force in the absence of heparin. Aprotinin-heparin-platelet interactions may help explain aprotinin's ability to reduce blood loss during CPB.
抑肽酶可干扰肝素与血小板的结合，并减少体外循环（CPB）期间的失血量。肝素可消除CPB期间的血小板力，而鱼精蛋白给药后血小板力的恢复程度似乎与失血量相关。本研究评估了抑肽酶对肝素抑制血小板力的影响。
使用Hemodyne止血分析仪测量血小板力。通过添加巴曲酶和10 mM氯化钙，由富含血小板血浆（PRP）形成凝块。凝血条件包括pH 7.4、离子强度0.15 M、纤维蛋白原水平1 mg/ml和75,000个血小板/微升。
凝血1200秒后，0.2 U/ml肝素使力从7110±1190 dyn降至450±450 dyn。添加抑肽酶[20微克/毫升（140 KIU/毫升）]的PRP中的血小板力未被肝素抑制（7480±2410 dyn）。向先前肝素化的血浆中添加抑肽酶[40微克/毫升（280 KIU/毫升）]可抵消肝素对力的抑制作用。在不含肝素的PRP中，抑肽酶（40微克/毫升）使血小板力从5630 dyn增加至11,138±562 dyn。抑肽酶不影响凝血酶活性、纤维蛋白结构、血小板聚集或分泌。
抑肽酶可抵消肝素对血小板力的抑制作用，并在无肝素的情况下增强血小板力。抑肽酶 - 肝素 - 血小板相互作用可能有助于解释抑肽酶在CPB期间减少失血量的能力。
