Landolfi R, De Candia E, Rocca B, Ciabattoni G, Antinori A, Masetti R, Patrono C
Hemostasis Research Center, Catholic University of Rome, Italy.
Thromb Haemost. 1994 Dec;72(6):942-6.
Several "in vitro" and "in vivo" studies indicate that heparin administration may affect platelet function. In this study we investigated the effects of prophylactic heparin on thromboxane (Tx)A2 biosynthesis "in vivo", as assessed by the urinary excretion of major enzymatic metabolites 11-dehydro-TxB2 and 2,3-dinor-TxB2. Twenty-four patients who were candidates for cholecystectomy because of uncomplicated lithiasis were randomly assigned to receive placebo, unfractionated heparin, low molecular weight heparin or unfractionated heparin plus 100 mg aspirin. Measurements of daily excretion of Tx metabolites were performed before and during the treatment. In the groups assigned to placebo and to low molecular weight heparin there was no statistically significant modification of Tx metabolite excretion while patients receiving unfractionated heparin had a significant increase of both metabolites (11-dehydro-TxB2: 3844 +/- 1388 vs 2092 +/- 777, p < 0.05; 2,3-dinor-TxB2: 2737 +/- 808 vs 1535 +/- 771 pg/mg creatinine, p < 0.05). In patients randomized to receive low-dose aspirin plus unfractionated heparin the excretion of the two metabolites was largely suppressed thus suggesting that platelets are the primary source of enhanced thromboxane biosynthesis associated with heparin administration. These data indicate that unfractionated heparin causes platelet activation "in vivo" and suggest that the use of low molecular weight heparin may avoid this complication.
多项“体外”和“体内”研究表明，给予肝素可能会影响血小板功能。在本研究中，我们通过主要酶代谢产物11-脱氢-TxB2和2,3-二去甲-TxB2的尿排泄量评估，研究了预防性肝素对“体内”血栓素（Tx）A2生物合成的影响。24例因单纯性结石而拟行胆囊切除术的患者被随机分配接受安慰剂、普通肝素、低分子量肝素或普通肝素加100mg阿司匹林治疗。在治疗前和治疗期间对Tx代谢产物的每日排泄量进行测量。在给予安慰剂和低分子量肝素的组中，Tx代谢产物排泄量无统计学上的显著改变，而接受普通肝素的患者两种代谢产物均显著增加（11-脱氢-TxB2：3844±1388 vs 2092±777，p<0.05；2,3-二去甲-TxB2：2737±808 vs 1535±771 pg/mg肌酐，p<0.05）。在随机接受小剂量阿司匹林加普通肝素治疗的患者中，两种代谢产物的排泄量被大大抑制，这表明血小板是与肝素给药相关的血栓素生物合成增强的主要来源。这些数据表明普通肝素在“体内”引起血小板活化，并提示使用低分子量肝素可能避免这种并发症。
