The Experimental Study On The Mechanism Of Delayed Brain Damage From Iron Overloading In Rat Intracerebral Haemorrhage

CHAPTER ONETHE MECHANISM OF IRON INSULTS FROMERYTHROCYTE LYSIS AFTER RATINTRACEREBRAL HAEMORRHAGE AND THE ROLEOF DEFEROXAMINE INTERVENTIONObjective: The mechanism of the delayed brain damage after intracerebral hemorrhage(ICH) is complicated and not well understood. ICH results in an accumulation of iron in the brain that possibly contributes to brain delayed insults and severe neurological deficits post-hemorrhage. So It is significant to study on mechanism of iron toxic process and intervention in ICH. The specific mechanism of brain edema is unclear at present. The water channels may be a key factor in brain edema. Deferoxamine(DFO) - a potent iron chelator can relieve brain edema resulted from ICH and hemoglobin. At present there were no research about the relations between iron overloading and water regulators. Without reports about relations between rate-limiting enzyme of iron release and oxidation/antioxidation,water regulators. No data of the other possible mechanisms of deferoxamine except its iron chelation to inhibit iron direct toxication. In our experiments, by means of surveying iron sediments and brain edema, water regulator, iron release enzyme, oxidation stress and antioxidation materials in different time after intracerebral hemorrhage and their spatio- temporal relations, to explore the mechanism of delayed brain insults result from iron -a major toxic product of erythrocyte lysis and the role of deferoxamine intervention in rat ICH models with autologous blood.Methods: ICH was established by infusing autologous blood into rat putamina;DFO intervention models was made by intraceliac injection with DFO 50mg bid; Observe the pathological changes ,irons aggradation...