Loskutoff D J
J Clin Invest. 1979 Jul;64(1):329-32. doi: 10.1172/JCI109457.
The vascular endothelium is a rich source of plasminogen activator (PA) and thus of blood vessel-associated fibrinolytic activity. Cultured bovine aortic endothelial cells were employed to determine if components of the coagulation system interact with the endothelium to modify expression of this activity. The addition of thrombin to these cultures led to a rapid decline in intracellular PA activity, with as little as 3 ng/ml, or 0.1 nM thrombin causing a 50% decrease within 30 min. Thrombin inactivated with diisopropylflurophosphate or hirudin did not elicit the response. Although control cultures secreted high levels of PA, no PA activity could be detected in the media surrounding the thrombin-treated cells. This loss of activity did not appear to result from direct inactivation of PA by thrombin. These observations indicate that the fibrinolytic potential of cultured endothelial cells is rapidly suppressed by trace amounts of thrombin. The generation of thrombin at sites of vascular injury may have a similar effect on the endothelium.
血管内皮是纤溶酶原激活物（PA）的丰富来源，因此也是与血管相关的纤溶活性的丰富来源。采用培养的牛主动脉内皮细胞来确定凝血系统的成分是否与内皮相互作用以改变这种活性的表达。向这些培养物中添加凝血酶会导致细胞内PA活性迅速下降，低至3 ng/ml或0.1 nM凝血酶在30分钟内可导致50%的下降。用二异丙基氟磷酸或水蛭素灭活的凝血酶不会引发该反应。尽管对照培养物分泌高水平的PA，但在凝血酶处理细胞周围的培养基中未检测到PA活性。这种活性丧失似乎不是由凝血酶直接使PA失活导致的。这些观察结果表明，微量凝血酶可迅速抑制培养的内皮细胞的纤溶潜力。血管损伤部位凝血酶的产生可能对内皮有类似作用。
