Owens M R, Cimino C D
Thromb Res. 1983 Jul 1;31(1):135-43. doi: 10.1016/0049-3848(83)90014-2.
The effects of sodium salicylate on synthesis of a vitamin K-dependent plasma coagulation protein, Factor II (prothrombin) was studied using the isolated rat liver perfused for 10 hours in vitro. Cumulative synthesis of Factor II was measured by a standard coagulation assay, by activation with E. carinatus venom, and by rocket immunoelectrophoresis. When sodium salicylate 5 mg or 25 mg was added to the liver perfusate (volume 100 ml) at the outset of the perfusion, cumulative synthesis of both coagulation activity and immunoreactive protein was significantly less than that seen in control perfusions containing no salicylate. The inhibitory effect of salicylate was prevented by pretreatment of rat liver donors with supplemental vitamin K injected 24 hours before sacrifice. Although some interaction between salicylate and vitamin K was apparent from these experiments, the results from vitamin K-deficient rat liver donors were quite different from those containing salicylate. There was no assayable Factor II coagulation activity produced in 10 hours of perfusion of vitamin K-deficient rat livers, but cumulative synthesis of immunoreactive Factor II was quite comparable to that seen in control perfusions.
利用体外灌注10小时的离体大鼠肝脏，研究了水杨酸钠对维生素K依赖性血浆凝血蛋白——因子II（凝血酶原）合成的影响。通过标准凝血试验、用角蝰蛇毒激活以及火箭免疫电泳法来测定因子II的累积合成量。在灌注开始时，当向肝脏灌注液（体积100毫升）中加入5毫克或25毫克水杨酸钠时，凝血活性和免疫反应性蛋白的累积合成量均显著低于不含水杨酸钠的对照灌注实验中的合成量。在处死大鼠前24小时给肝脏供体注射补充维生素K进行预处理，可防止水杨酸盐的抑制作用。尽管从这些实验中可以明显看出水杨酸盐与维生素K之间存在一些相互作用，但维生素K缺乏的大鼠肝脏供体的实验结果与含有水杨酸盐的实验结果截然不同。维生素K缺乏的大鼠肝脏灌注10小时未产生可检测到的因子II凝血活性，但免疫反应性因子II的累积合成量与对照灌注实验中的相当。
