| Intracerebral hemorrhage (ICH) includes traumatic intracerebral hemorrhage(TICH) and spontaneous intracerebral hemorrhage(SICH). There is a significant brain edema around intracerebral hematoma in clinic, but its cause is not completely known now. In the past, the development of brain edema after ICH was considered to be associated with space-occupying effect and disturbance of blood circulation. Now many studies show that some substances from blood clot and blood components can be responsible for brain edema production. However, these studies have two limits:(l) the study of brain edema formation after ICH is focused on SICH now, that is only study the relationship between blood components and brain edema when the animals are not subjected to brain injury;(2) the relationship between blood components in blood circulation and brain edema is studied when the animals are subjected to brain injury. Recent studies show that erythrocyte and its breakdown products play an important role in formation of brain edema following ICH through heme from lysed erythrocyte. Metabolism of heme by heme oxygenase (HO) after red blood cell(RBC) lysis results in the results in the release of iron, carbon monoxide and bilirubin, which damage brain tissue by free radicals and lipid peroxidation and produce brain edema. In addition, RBC of hematoma also activates tumor necrosis factor-a(TNF-a), which damage blood-brain barrier(BBB) and worsen brain edema. However, up to now we don't find the reportabout relationship between blood components and brain edema following TICH. Erythrocyte is the most blood cell in blood, so we study the role of RBC on brain edema development after TICH and offer some experimental bases for clinical treatment and scientific research of TICH.Part 1 Effects of erythrocyte on brain edema following traumaticintracerebral hemorrhageObjective:To set up animal model of TICH in SD rat and observe the effects of erythrocyte on brain edema after TICH. Methods: Sixty healthy adult SD rats were randomly divided into four groups, 15 in each one. The animals subjected to traumatic brain injury(TBI) were acted as controlled group, and experimental groups consisted of three groups, which suffered from TBI and received cortical injection of whole blood(WB), lysed RBC(LRBC), or packed RBC(PRBC). Firstly, the model of brain injury was established by applying a free-falling device in rats, then WB,LRBC or PRBC were infused with stereotactic guidance into injuried cortex to produce model of TICH. Each group was further divided into three subgroups at 1 day, 3days or 5 days after brain injury, 5 in each one. All rats were killed at 1 day, 3days or 5 days after injury, measured water content, levels of sodium, potassium and calcium in brain tissue, and observed pathological changes with light microscope and electron microscope. Results: 1.Water content: The brain water content at the third day was significantly higher than that at the first day and at the fifth day in group of WB, PRBC or TBI(P<0.05orP<0.01). Brain water content of LRBC 1 was markedly higher than that of LRBC 3(P<0.05) and LRBC 5(P<0.01). Comparison among four groups, watercontent of LRBC was the highest at 1 day (P<0.01), and that of WB and PRBC were the highest at 3 days (P<0.01), and there was no significant difference among that of 4 groups at 5 days. 2. Level of ion. The change of Na+ coincided with that of water content, that was which group water content significantly increased had Na+ markedly increased. There was a less concord of decrease of K+ and increase of water content. There was no relationship between level of Ca2+ and water content. 3. Pathological manifestation: Naked observation, all of the animals had the same focal contusion and laceration of brain, subarachnoid hemorrhage(SAH) and cortex edema around injuried area. There were hematoma inside cortex and edema around hematoma at coronal surface of WB, LRBC or PRBC. At the first day postinjury, the main pathological changes after brain injury, WB and PRBC group...
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