次声作用后脑组织环核苷酸与TXA_2、PGI_2代谢改变及意义

CHANGS IN CYCLIC NUCLEOTIDES ,TXA_2 AND PGI_2 METABOLISM AFTER INFRASONIC DAMAGE AND THEIR SIGNIFICANCE

本研究探讨次声作用后脑皮层组织环核甘酸与花生四烯酸代谢产物血栓素A2 (TXA2 )和前列环素(PGI2 )代谢改变及意义。将 40只SD大鼠随机分为正常对照、次声作用 1次、7次、1 4次及代谢性谷氨酸受体拮抗剂α 甲基 4 羧基苯氨基乙酸 (MCPG)治疗 5组。采用本校研制的次声压力仓。次声作用组用 8Hz、1 2 0dB的次声按规定次数 ,每次作用 2h。各组到预定时间后 ,取脑组织匀浆 ,用放免进行环磷酸腺苷 (cAMP)、环磷酸鸟苷(cGMP)与TXB2 及 6 酮 (TXA2 、PGI2 稳定代谢产物 )含量测定 ,并对脑组织匀浆进行蛋白定量。结果 :cAMP、cGMP与TXB2 及 6 酮含量 ,在次声作用 1次组 ,无显著改变 ;在 7次与 1 4次组 ,cAMP与TXB2 含量显著升高 (P<0 .0 1 ) ,6 酮含量明显降低 (P <0 .0 1 )。TXB2 /6 酮比值呈递增趋势 ;治疗组 :cAMP、TXB2 及 6 酮含量与TXA2 /PGI2 比值有明显恢复。提示次声可以通过引起脑cAMP、cGMP与TXA2 、PGI2 代谢改变造成脑损害 ,这是次声导致脑损害的重要因素之一。在相同强度的次声的作用下 ,作用次数的多少与脑cAMP、cGMP与TXA2 、PGI2 代谢改变程度呈直接相关关系。MCPG可能通过影响脑cAMP与TXA2 、PGI2 代谢改变而起脑保护作用。

To study the changes in cyclic nucleotides, TXA 2 and PGI 2 metabolism after infrasonic damage to the rats so as to probe into the mechanism of infrasonic biologic effects. 40 SD rats were randomizied into control, infrasonic damage 1 time, 7 times, 14 times and treatment groups. Eight Hz、120dB infrasound was applied to infrasounic groups for 2h once according to the planned times. Immunoradioassay was used for the examination of brain cAMP, cGMP, TXB 2 and 6 keto PGF1a(metabolites of TXA 2 and PGI 2) contents. It showed that there were no changes in cAMP、cGMP, TXB 2 and 6 keto PGF1a levels in 1 time group while cAMPand TXB 2 level elevated significantly and 6 keto PGF1a level decreased remarkably in 7 and 14 times groups with a augmented TXA 2/PGI 2 value. In treatment group cAMP, TXB 2 and PGI 2 levels became normal. It is concluded that the augmentation of TXA 2/PGI 2 value in 7 and 14 times groups suggests that an imbalance in TXA 2 PGI 2 production contributes to brain injury, which includes ischemia and edema. The extent of cAMP, cGMP, TXA 2 and PGI 2 metabolism disturbance is closely related to the times of infrasonic injury. And it is hypothesized that mGluR antagonist may exert its protective effect by increasing PGI 2 production and improving blood supply to the injured blood vessels.