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目的探讨急性低压缺氧时血栓素A2(TXA2)和前列环素(PGI2)的变化及其与脑血流量变化的关系。方法将20只大鼠随机分为常氧对照组(n=10)和急性低压缺氧组(n=10),用电磁血流量计测定脑血流量,用放免法分别测量TXA2、PGI2的含量。由于TXA2和PGI2的不稳定性,目前推以直接测定,故国内外均以测定其代谢产物TXB2、6-keto-PGF1α作为判断其浓度的指标。结果急性低压缺氧时脑血流量、脑含水量、血浆、脑组织TXB2含量、脑组织TXB2/6-keto-PGF1α比值明显增高(P<0.05),6-keto-PGF1α无明显变化。结论急性低压缺氧时,TXA2、脑血流量均增加,TXA2参与了急性低压缺氧时脑血流量的调节,可能以抑制脑血管过度扩张作用为主。
Objective To investigate the changes of TXA2 and PGI2 in acute hypobaric hypoxia and its relationship with changes of cerebral blood flow. Methods Twenty rats were randomly divided into normoxia control group (n = 10) and acute hypobaric hypoxia group (n = 10). The cerebral blood flow was measured by electromagnetic flowmeter and the levels of TXA2 and PGI2 . Due to the instability of TXA2 and PGI2, the current push to direct determination, so both at home and abroad to determine its metabolites TXB2, 6-keto-PGF1α as an indicator of its concentration. Results Acute hypobaric hypoxia showed a significant increase in cerebral blood flow, brain water content, TXB2 content in plasma and brain tissue, TXB2 / 6-keto-PGF1α ratio (P <0.05), and no significant change in 6-keto-PGF1α. Conclusion When acute hypobaric hypoxia, TXA2 and cerebral blood flow are both increased. TXA2 is involved in the regulation of cerebral blood flow during acute hypobaric hypoxia, which may be mainly due to the inhibition of excessive cerebral dilation.