Badylak S F, Poehlman E, Williams C, Klabunde R E, Turek J, Schoenlein W
Hillenbrand Biomedical Engineering Center, Purdue University, W. Lafayette, IN 47907.
J Pharmacol Methods. 1988 Jul;19(4):293-304. doi: 10.1016/0160-5402(88)90003-4.
Three separate studies were done to evaluate a new canine model of arterial thrombosis with endothelial injury. Endothelial injury was produced by exposing the luminal surface of a 2-cm segment of femoral artery to 100 degrees C saline for 5 min. There was no disruption of proximal or distal blood flow with this model, and thrombolysis was continuously monitored by measuring 125I-labelled fibrin gamma emissions from the thrombus. Study No. 1 showed that complete endothelial denudation was achieved with this model. Study No. 2 demonstrated 1) adherence of the experimentally induced thrombus to subendothelial connective tissue, and 2) endogenous thrombolysis of approximately 9% during the initial 2 h after thrombus formation. Study No. 3 tested the usefulness of the model for evaluating the thrombolytic efficacy of urokinase. Urokinase (30,000 U/Kg, bolus IV injection) caused 38 +/- 5.4% thrombolysis within 90 min of drug administration versus 5.9 +/- 2.4% for a saline-treated control group. We conclude that this model provides a technically simple and reproducible method for the laboratory investigation of thrombosis and thrombolysis in arteries with endothelial injury.
开展了三项独立研究以评估一种新的伴有内皮损伤的犬动脉血栓形成模型。通过将一段2厘米长的股动脉管腔表面暴露于100摄氏度的盐水中5分钟来造成内皮损伤。该模型不会破坏近端或远端血流，并且通过测量血栓中125I标记的纤维蛋白γ射线发射来持续监测溶栓情况。研究1表明该模型可实现完全内皮剥脱。研究2证实了1）实验诱导的血栓与内皮下结缔组织的黏附，以及2）血栓形成后的最初2小时内约9%的内源性溶栓。研究3测试了该模型在评估尿激酶溶栓疗效方面的实用性。尿激酶（30,000 U/Kg，静脉推注）在给药后90分钟内导致38±5.4%的溶栓，而盐水处理的对照组为5.9±2.4%。我们得出结论，该模型为伴有内皮损伤的动脉血栓形成和溶栓的实验室研究提供了一种技术上简单且可重复的方法。
