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 solu...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 PGF1α (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 PGF1α 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).展开更多
文摘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 PGF1α (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 PGF1α 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).
