Wojta J, Jones R L, Binder B R, Hoover R L
Department of Pathology, Vanderbilt University, Nashville, TN 37232.
Blood. 1988 Jun;71(6):1703-6.
The effect of anoxia on the fibrinolytic potential of cultured endothelial cells derived from bovine pulmonary artery and bovine lung microvasculature was studied. Both cell types reacted with an increase in plasminogen activator inhibitor (PAI) activity and a decrease in the plasminogen activator (PA) activity in the media after incubation under anoxic conditions. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis followed by fibrin autography and reverse fibrin autography indicated that the change in fibrinolytic potential was due to an impaired release of PA and not an increase in the production of PAI. Although anoxia did not affect the viability of the cells as judged by 51Cr release, their metabolism was influenced, which is reflected by increases in the levels of lactate in cell lysates and media. Furthermore, the effect of short-term anoxia on PA and PAI could not be reversed by reoxygenation for 24 hours. The results are discussed in terms of helping to explain the tendency of reocclusion after successful thrombolytic therapy, the development of pulmonary hypertension, and the thrombotic tendency of areas with an impaired circulatory supply.
研究了缺氧对源自牛肺动脉和牛肺微血管的培养内皮细胞纤溶潜力的影响。在缺氧条件下孵育后，两种细胞类型均表现为培养基中纤溶酶原激活物抑制剂（PAI）活性增加，纤溶酶原激活物（PA）活性降低。十二烷基硫酸钠-聚丙烯酰胺凝胶电泳，随后进行纤维蛋白自显影和反向纤维蛋白自显影表明，纤溶潜力的变化是由于PA释放受损，而非PAI产生增加。尽管通过51Cr释放判断缺氧并未影响细胞活力，但其代谢受到影响，这表现为细胞裂解物和培养基中乳酸水平升高。此外，短期缺氧对PA和PAI的影响在复氧24小时后无法逆转。从有助于解释成功溶栓治疗后再闭塞的倾向、肺动脉高压的发展以及循环供应受损区域的血栓形成倾向等方面对结果进行了讨论。
