Abstract
In this paper we study the changes and significance of the TXA2 and PGI2 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 TXB2 and 6-keto-PGF1a (metabolites of TSA2 and PGI2) contents. The results showed that there were no changes in TXB2 and 6-keto-PGF1a levels in the ‘once’ group while TXB2 level elevated significantly and 6-keto-PGF1a level decreased remarkably in the 7 times and the 4 times groups with an augmentation of TXA2/PGI2 value. In the treatment group both TXB2 and PGI2 levels nearly reached normal. It is concluded that the augmentation of the TXA2/PGI2 value in the 7 times and 14 times groups suggests that an imbalance in TXA2-PGI2 production contributes to the traumatic secondary processes, which include ischemia and edema. Also, the extent of TXA2 and PGI2 metabolism disturbance is closely related to the times of infrasonic injury. It is hypothesized that mGluR antagonist may exert its protective properties through increasing PGI2 production in the injured brain by improving the blood supply to injured blood vessels.