The Changes and Significance of TXA2 and PGI2 Metabolism after Rat Infrasonic Brain Damage

In this paper we study the changes and significance of the TXA 2 and PGI 2 metabolism after infrasonic damage to rats so as to probe the mechanism of infrasonic biological effects. Some 40 SD rats were randomized into control, infrasonic damage once, 7 times, 14 times, and treatment five groups. A stimulus of 8Hz 120dB infrasound was applied to the infrasonic damage groups for 2 hours once according to the planned times. Radioimmunoassay was used for the examination of brain TXB 2 and 6-keto-PGF1a (metabolites of TSA 2 and PGI 2 ) contents. The results showed that there were no changes in TXB 2 and 6-keto-PGF1a levels in the ‘once’ group while TXB 2 level elevated significantly and 6-keto-PGF1a level decreased remarkably in the 7 times and the 4 times groups with an augmentation of TXA 2 /PGI 2 value. In the treatment group both TXB 2 and PGI 2 levels nearly reached normal. It is concluded that the augmentation of the TXA 2 /PGI 2 value in the 7 times and 14 times groups suggests that an imbalance in TXA 2 -PGI 2 production contributes to the traumatic secondary processes, which include ischemia and edema. Also, the extent of TXA 2 and PGI 2 metabolism disturbance is closely related to the times of infrasonic injury. It is hypothesized that mGluR antagonist may exert its protective properties through increasing PGI 2 production in the injured brain by improving the blood supply to injured blood vessels.