Doni M G, Piva E
Thromb Haemost. 1983 Jun 28;49(3):228-9.
A study was performed to evaluate the hypothesis that heparin opposes uncontrolled PGI2 production by vessels due to thrombin generation. We treated animals with warfarin, an inhibitor of liver synthesis of prothrombin and other vit. K-dependent clotting factors. In fact, if thrombin is presumed to be the stimulus for PGI2 production, warfarin should suppress this effect. As warfarin treatment did not affect significantly PGI2-like activity, we conclude that a different hypothesis is necessary to explain the phenomenon. On the other hand, i.p. sodium heparin effectively induced a decrease in PGI2-LA synthesis, whereas s. c. calcium heparin did not significantly influence it.
肝素可对抗因凝血酶生成导致的血管不受控制的前列环素(PGI2)生成。我们用华法林治疗动物,华法林是肝脏合成凝血酶原及其他维生素K依赖性凝血因子的抑制剂。事实上,如果假定凝血酶是PGI2生成的刺激因素,那么华法林应该会抑制这种作用。由于华法林治疗并未显著影响类PGI2活性,我们得出结论,需要一个不同的假说才能解释该现象。另一方面,腹腔注射肝素钠可有效诱导PGI2-LA合成减少,而皮下注射肝素钙对其没有显著影响。