Abstract:
Crush syndrome develops due to muscle crush injury often found in patients extricated from prolonged compression after disasters. It leads to rhabdomyolysis, kidney failure and hypovolemic shock, followed by decreased blood supply, to tissue under compression and general body parts including brain. In the present study, experimental model of crush syndrome in albino rats was induced by, 2 h of compression followed by 48 h of decompression, of femoral muscle tissue. Aspartate and alanine aminotransferase activities of rat brain regions during crush syndrome were investigated. After exposure to 2 h compression in comparison to normal/control levels, both cytosolic AST and ALT activities reduced. Cytosolic AST activity reduced by 31.2 percent, 26.1 percent and 19.4 percent in olfactory lobes, cerebral cortex and cerebellum, respectively, whereas cytosolic ALT activity decreased by 51.1 percent, 52.4 percent, 47.4 percent and 36.9 percent in olfactory lobes, cerebral cortex, cerebellum and medulla oblongata, respectively.
