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期刊论文
Brain edema after experimental intracerebral hemorrhage: role of hemoglobindegradation products
J Neurosurg 96: 287-293, 2002,-0001,():
Object The mechnisms involved in brain edema formation following intracerebral hemorrhage (ICH) have not been fully elueidated. The authous have found that red blood cell lysis plays an important role in edema develop-ment after ICH. In the present study, they soughy to detennine whether degradation produets of hemoglobin cause brain edema. Methods Hemoglobin, hemin, bilirubin, of FeCL2, were in fused with stereotactie guidance into the right basal gan-glia of Sprague-Dawley rats. The animals 24 hours later to determine brain water and ion contents. Wesern blot analysis and immunohistochemistry were applied for heme oxygenase-1 (HO-1) measurement. The effects of an HO inhibitor, tin-protoporphyrin (SnPP), and the iron chelator deferoxamine, on hemoglobin-induced brain edema were also examined. Intracerebral infusion of hemoglobin, hemin, bilirubin, or FeCl2 cansed an inerease in brain water content at 24 hours, The HO-1 was upregulated after hemoglobin infusion and HO inhibition by Snpp-attenuated hemoglobin in duced edema. Brain edema induced by hemoglobin was so attenuated by the intraperitoneal injection of 500mg/kg deferoxamine. Conchusions Hemoglobin causes brain edema. at least in part, through its degradation products. Limiting hemo-globin degradation coupled with the use o9f iron chelator may be a novel therapeutie approach to limit brain edema after ICH.
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