OBJECTIVE: The brain TXA(2) and PGI(2) levels in a new rodent model of impact acceleration diffuse brain injury alone and with hypotention and hyperthermia in combination were observed to look into the relationship between TXA(2), PGI(2) levels and different types of head injury. METHODS: Thirty-two SD rats were randomized into sham, head injury alone, secondary insult alone and head injury with secondary insult groups. At 4 hours after injury or experiment, all the rats were decapitated and their brains were sampled for radioimmunoassay (RIA) measurement. RESULTS: Compared with that of sham group there were no changes in TXA(2) and PGI(2) levels in injury alone group while there was a significant augmentation in PGI(2) level in insult alone group. Both TXA(2) and PGI(2) level in injury with secondary insult group increased significantly in comparison with that of sham at 4 hours postimpact. CONCLUSIONS: PGI(2) providing energy and precursors to the injured tissue and producing some vasoactive arachidonic products, especially TXA(2), is closely connected to the severity of brain damage.

OBJECTIVE: To study the changes of brain TXA(2) and PGI(2) levels in a new rodent model of impact acceleration diffuse brain injury with hypotention and hypoxia and the effect of diaspirin cross linked hemoglobin solution (DCLHb) on brain TXA(2) and PGI(2) levels. METHODS: Thirty-two male SD rats were randomized into sham, head injury alone, head injury with secondary insults and injury with insults followed by DCLHb administration groups. Animals were physiologically monitored throughout the experiment and the prostanoids were measured via radioimmunoassay (RIA). RESULTS: There were no changes in TXB(2) and 6-keto-PGF1alpha (stable metabolites of TXA(2) and PGI(2)) levels in injury alone group while TXB(2) level in secondary insults group elevated significantly and both TXB(2) and 6-keto-PGF1alpha levels in injury with insults followed by DCLHb administration augmented significantly in comparison with the corresponding value of sham at 4 h postimpact. CONCLUSIONS: The only increase in TXA(2) level in secondary insults rats suggests that there may be both thrombotic episodes and vasoconstriction leading to focal increase in micro-circulatory resistance which contributes to a decreased focal cerebral blood flow (CBF). And it is hypothesed that DCLHb may exert its protective properties through increasing PGI(2) production in injured brain by affecting CBF and cerebral perfusion pressure (CPP).