论文部分内容阅读
目的:探讨实验性大鼠肺血栓栓塞前后血浆TXA2,PGI2和T/P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T/P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TXB2 3h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),T/P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T/P比值失衡在PTE的早期病理生理过程中发挥重要作用。
Objective: To investigate the changes and significance of plasma TXA2, PGI2 and T / P ratio in experimental rats before and after pulmonary thromboembolism. Methods: Sixty healthy Wistar rats were randomly divided into embolization group, embolization for 1h, 3h, 5h, 7h, 12 rats in each group. Pulmonary thromboembolism model was established by injecting 2ml autologous thrombus suspension into the embolization group, Arterial blood was collected before embolization and at 1h, 3h, 5h and 7h after embolization. Arterial blood gas analysis and radioimmunoassay were used to detect TXB2, 6-Keto-PGF1α and T / P ratio. Results: The histopathology was in accordance with the change of pulmonary thromboembolism. The PO2 of embolization group was significantly higher than that of preembolization group (P <0.01), the peak of plasma TXB2 reached the peak at 3 h, and the 6-Keto-PGF1α gradually increased from baseline to 7 h (P <0.01). There was an imbalance between T / P ratio and peak value at 1h. Conclusion: The establishment of autologous pulmonary embolism model in rats is successful. The imbalance of TXA2 and T / P ratio plays an important role in the early pathophysiological process of PTE.