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目的 探讨次声作用后脑皮层组织血栓素A2 (TXA2 )、前列环素 (PGI2 )代谢改变及及代谢性谷氨酸受体拮抗剂MCPG的作用。方法 40只SD大鼠随机分为正常对照、次声作用 1次、7次、14次及代谢性谷氨酸受体拮抗剂MCPG治疗 5组。采用第四军医大学研制的次声压力仓。用 8Hz、12 0dB的次声按规定次数 ,每次作用 2h。采用蛋白定量和放免法行脑TXA2 、PGI2 稳定代谢产物血栓素B2 (TXB2 )及 6 酮 PGF1α( 6 酮 )含量测定。结果 7次与 14次组 ,TXB2 含量有显著意义升高 (P <0 .0 1) ,6 酮含量明显降低 (P <0 .0 1)。TXA2 /PGI2 值呈递增趋势 ;治疗组 ,TXB2 及 6 酮含量与TXA2 /PGI2 值恢复致正常水平。结论 次声可以通过引起脑TXA2 、PGI2 代谢改变造成脑损害 ,是次声导致脑损害的关键因素之一。MCPG可能通过影响脑TXA2 、PGI2 代谢改变而起脑保护作用。
Objective To investigate the effects of infrasound on the metabolism of thromboxane A2 (TXA2), prostacyclin (PGI2) and the metabotropic glutamate receptor (MCPG). Methods Forty Sprague Dawley rats were randomly divided into normal control, infrasound acupuncture treatment once, seven times, 14 times and metabolic glutamate receptor antagonist MCPG treatment five groups. Infrasound pressure chamber developed by the Fourth Military Medical University. With 8Hz, 12 0dB infrasound by the required number of times, each role 2h. The content of thromboxane B2 (TXB2) and 6-keto PGF1α (6-keto), the brain metabolites of TXA2 and PGI2, were determined by protein quantification and radioimmunoassay. Results 7 and 14 groups, TXB2 content was significantly increased (P <0. 01), 6 ketone content decreased significantly (P <0.01). TXA2 / PGI2 value showed an increasing trend; the treatment group, TXB2 and 6 ketone content and TXA2 / PGI2 values returned to normal levels. Conclusion Infrasound can cause brain damage by causing metabolic changes of brain TXA2 and PGI2, which is one of the key factors of infrasound-induced brain damage. MCPG may play a neuroprotective role by affecting the metabolism of TXA2 and PGI2 in the brain.