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目的探讨实验性大鼠肺血栓栓塞血浆TXA2,PGI2浓度和TXA2,PGI2比值的变化及意义。方法健康Wistar大鼠60只,随机分为栓塞前组,栓塞1h,3h,5h,7h组,每组12只,栓塞组自颈外静脉注入自体血栓混悬液2ml建立肺血栓栓塞模型,栓塞前和注栓后1h,3h,5h,7h各时点收集动脉血,进行动脉血气分析和用放免法检测TXB2,6-Keto-PGF1α及TXA2,PGI2比值。结果组织病理符合肺血栓栓塞的改变;栓塞组注栓后PO2较栓塞前组比较差异显著(P<0.01);血浆TXB23h达高峰值,6-Keto-PGF1α从基线逐渐上升至7h时点达高峰值,二者各时点与栓塞前比较差异有显著性(P<0.01),TXA2,PGI2比值失衡,1h时点达高峰值。结论建立大鼠自体肺栓塞模型成功;缩血管因子TXA2和TXA2,PGI2比值失衡在PTE的初始和早期病理生理过程中发挥重要作用。PGI2对PTE后期病理生理过程有重要影响。
Objective To investigate the changes and significance of TXA2, PGI2 and TXA2, PGI2 in experimental rat pulmonary thromboembolism. Methods Sixty healthy Wistar rats were randomly divided into pre-embolization group, embolization of 1h, 3h, 5h, 7h group, 12 rats in each group. Pulmonary thromboembolism model was established by embolization of 2ml self- Arterial blood was collected before and 1h, 3h, 5h and 7h after injection. Arterial blood gas was collected and the ratios of TXB2, 6-Keto-PGF1α, TXA2 and PGI2 were measured by radioimmunoassay. Results The histopathology was consistent with the change of pulmonary thromboembolism. The PO2 of embolization group was significantly higher than that before embolization (P <0.01), the peak of plasma TXB23h and the peak of 6-Keto-PGF1α gradually increased from baseline to 7h (P <0.01). The ratios of TXA2 and PGI2 were unbalanced, and peaked at 1h. Conclusion The establishment of autologous pulmonary embolism model in rats is successful. The imbalance of TXA2, TXA2 and PGI2 plays an important role in the initiation and early pathophysiology of PTE. PGI2 plays an important role in the pathophysiology of PTE.