| Objectives: ICH is one of commonly and frequently encountered diseases in cerebrovascular diseases ,significantly threatens human health。It accounts for 10%-20% of all acute cerebrovascular diseases,its morbidity mortality and disability rate are higher than others, stroke diseases。No definitely conservative treatment is available for ICH. ICH fatality is 70% to 80%。Brain edema after ICH is one of reasons which lead to disease aggravation and one of hot spots which is researched by domestic and foreign experts. Blood components (especial thrombinogen) and cerebral ischemia induced by ICH besides acute location effect are the important reasons. Most researchers believe that the secondary injury around hematoma is the main cause which leads to the deterioration of nerve function. The most important pathophysiologic change is the secondary brain edema following ICH. The reason of brain edema formation is very complex. Hemoglobin release after erythrocyte cytolysis in the hematoma and inflammatory cytokines participation may be important reasons in brain edema formation after ICH. Cytokines are basic mediators of immunity,and involved the inflammatory cells activation and infiltration. The functions of cytokines are greatly complicated in vivo, affect each other in their induction, regulation of receptor, and exertion of bioactivity. So a sophisticated cytokine network was formed.In recent years,inflammatory cytokines TNF-a,IL-1,IL-6,IL-8 are important reasons in the brain edema formation after ICH. Some experiments identify IL-10 can inhibit synthesis and releasing of TNF-a,IL-6,IL-8 of macrophage and mononuclear cells。Now inflammatory cytokines are important in TCH condition progression and cerebral edema, which are identified by animal tests. Some foreign research identified the levels of IL-8,IL-10 in ICH patients are significantly high. The levels of IL-8 and IL-10 were assayed in venous serum and hematoma fluid in patients with cerebral hemorrhage to approach the mechanism of cerebral edema and identify if the levels of IL-8 and IL-10 in venous serum and hematoma fluid if are high , the relation with cerebral edema. if the levels of IL-8 and IL-10 induced by different hemorrhage volume are different. We further know the correlation of cytokines and cerebral edema, which had directed significance about the foundation research of cytokines and can supply theory evidence to research ICH medicine and operation opportunity.Methods: Eliminated standard:①infected or incorporated infection patients within 2w;②The patients were operated,injury within 6m;③The ICH patients induced by vascular malformation, vasculitis or clotting mechanism disorder;④The patients combining heart disease, nephrosis or tumor diseases;⑤DM and hyperlipemia;⑥The patients fell ill by TIA or stroke history in the near future.Contents of IL-6,IL-10 in venous serum and hematoma fluid were detected in 89 basal ganglion ICH patients after intracerebral hemorrhage, respectively, brain hematoma and edema around hematoma volume were measured through CT at the same time. The 89 ICH patients are divided into five groups( < 6h,6-12h,12-24h,24-72h,3-7d). Venous serum and hematoma fluid are collected at the same time. Brain hematoma and edema around hematoma volume were measured through CT according to Duotian formula in<6h patients. The levels of IL-8,IL-10 were compared with 17 healthy people serum IL-8,IL-10 contents。The blood was drew in the control group, which was about 3ml.The serum which involved in all specimen were isolated and conserved in -20℃frig. The levels of IL-8,IL-10 were quantitatively detected with kits and by ELISA method. Data was analysed by statistic methods of t-testing and correlation-regression analysis. All data were expressed as mean±SEM.Results:1 The levels of IL-8,IL-10 in venous serum and hematoma fluid are higher in the ganglion ICH group than that of the control group(P<0.05), The levels of IL-8,IL-10 in venous serum and hematoma fluid are coincident(P>0.05).The level of IL-8 has tendency to decrease within 6h,and reaches to peak at 24-72h and tends to decrease thereafter. However, its level remains significantly higher compared with that of control group. The level of IL-10 in venous serum and hematoma fluid tends to rises at 6-12h(which is compared with in the control group P<0.05),progressively increases thereafter. Brain edema volume around hematoma enlarges at 24h, reaches to peak at 3d ,tends to decrease thereafter, its level remains significantly higher compared with that of control group. Meanwhile IL-8 content keeps on the high level during this time. There is a closely relationship between IL-10 and IL-8 in serum, the peak of IL-8 emerges earlier than that of IL-10, the level of IL-8 is correlate with brain edema enlargement around hematoma.Conclusion:1 the level of IL-8,IL-10 in serum and hematoma fluid are significantly higher . IL-8,IL-10 may be involved in the pathophysiologic process of brain edema after ICH, brain changes damage of concentrations of IL-8,edema after ICH leads to IL-10, and aggravate brain around the hematoma.2 Serum IL-8 content shows serial changes in patients with ganglion intracerebral hemorrhage. High serum IL-6 content is harm to the brain edema around the hematoma.3 Serum IL-10 intracerebral content shows serial changes in patients with ganglion hemorrhage. There is no final conclusion how IL-10 concretely effect on edema around hematoma now. 4 The study have observed the serial changes of serum and the volume of brain edema around hematoma with intracerebral hemorrhage, may offer some support for the treatment of ICH.
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