TXA_2和PGI_2在实验性蛛网膜下腔出血迟发性血管痉挛中的作用

The effection of TXA_2 and PGI_2 to delayed cerebral vasospasm following experimental subarachnoid hemorrhage

目的观察花生四烯酸代谢产物血栓素A2(TXA2)合成酶特异性抑制剂奥扎格雷钠对实验性蛛网膜下腔出血(SAH)后TXA2和前列环素(PG I2)的影响,进一步探讨TXA2和PG I2在自发性蛛网膜下腔出血迟发性血管痉挛发生机制中的作用。方法将24只日本大耳白兔随机等分为2组:(1)SAH组(A组);(2)SAH+奥扎格雷钠治疗组(B组)。采用枕大池二次注血法建立兔SAH模型,B组在第1次注血后开始静脉输注奥扎格雷钠,每天给药1次,持续14d。全程观察两组实验动物的饮食及神经功能变化情况,利用放射免疫方法及CTA分别动态观察各组处理后1、4、7、11、14d的TXA2、PG I2及兔基底动脉直径。结果放射免疫检测TXA2发现B组较A组明显降低(P<0.05),而前列腺素B组较A组明显升高(P<0.05)。基底动脉直径测定的结果提示A组、B组无显著性差异(P>0.05);神经功能评分显示B组较A组改善明显(P<0.05)。结论TXA2和PG I2失调不是自发性蛛网膜下腔出血后迟发性血管痉挛主要发生机制。

Objective To observe the effection of ozagrel on TXA2 and PGI2 following experimental subarachnoid hemorrhage. And to investigate it＇ s mechanism in cerebral vasospasm. Methods Twenty-four white rabbits were divided into two groups randomly（ n = 12） ：Group A（SAH） ;Group B（ SAH ＋ ozagrel）. The ozagrelwas intravenously administrated daily from day 0 after first injection to day 14. In the whole range, neurologic assessments were performed on each day of scanning. The expression of TXA2 and PGI2in peripheral blood were measured by radio-immunity, and the diameters of basilar artery were measured by CT angiography on days 1,4,7,11 and 14 after the first injection. Results After treatment with ozagrel, the plasma levels of TXB2 in the group B were siginificantly reduced from that of the group A（ P 〈0.05 ） ,and the plasma levels of 6-Keto-PGF1α was increaced from that of the groupA（P 〈 0.05） ,there was not siginificant difference of the measurement of basilar artery diameter between the two groups;Neurologic scores in the ozagrel group were better than SAH group（P 〈0.05）. Conclusion The disturbancement of arachidonic acid metabolic product（TXA2和PGI2） is not main reason to cerebral vasospasm following experimental subarachnoid hemorrhage.