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作 者:李建立[1] 赵砚丽[1] 景吉林[2] 苏业璞[2]
机构地区:[1]河北省人民医院麻醉科,河北石家庄050051 [2]河北省人民医院心外科,河北石家庄050051
出 处:《中国体外循环杂志》2005年第2期70-73,共4页Chinese Journal of Extracorporeal Circulation
摘 要:目的探讨体外循环(CPB)导致全身炎症反应时致炎因子与抗炎因子的变化规律以及与机体免疫功能的关系,为临床防治全身炎症反应综合征(SIRS)提供实验依据。方法选取心内直视手术患者30例,用流式细胞仪测定单核细胞及淋巴细胞人类白细胞表面抗原-DR(HLA-DR)的表达,ELISA法测定血浆肿瘤坏死因子-α(TNF-α)和白介素-10(IL-10)浓度。结果CPB在导致炎症介质TNF-α升高的同时抗炎介质IL-10也随之升高,二者峰值出现的时间有一定差异,二者峰值呈正相关(r=0.698,P<0.01),CPB导致单核细胞HLA-DR表达下降,其随时间的变化趋势与IL-10相反。单核细胞HLA-DR最低值与CPB时间呈负相关(r=-0.489,P<0.05)。结论CPB导致炎症反应的同时抗炎反应也相继发生,炎症反应越强烈,抗炎反应也越强烈,机体免疫功能受损越为严重。CPB对机体的损伤是炎症反应与抗炎反应共同作用的结果。拮抗致炎因子的同时提高机体免疫功能维持致炎因子与抗炎因子平衡是治疗SIRS的新思路。OBJECTIVE To evaluate the kinetic changes of pro-inflammatory and anti-inflammatory cytokines to CPB and their relations to immunity function,and to give the experimental basis for treating SIRS.METHODS The HLA-DR expression on monocytes and lymphocytes were measured with Flow Cytometry . The plasma TNF-α and IL-10 concentration were determined by enzyme-linked immunosorbent assays.RESULTS The plasma TNF-α value began to elevate significantly after CPB and IL-10 value also increased significantly at the same time,the peaks of TNF-α and IL-10 were different, the TNF-α peak value correlated positively with IL-10 peak value(r=0.698,P<0.01).The HLA-DR expression on monocytes reduced after CPB, The change tendency with time was contrary to IL-10. Its lowest value correlated negatively with the duration of CPB (r=-0.489,P<0.05). CONCLUSION The inflammatory response and anti-inflammatory response to CPB occurred at the same time and the more serious inflammatory response was,the more serious anti-inflammatory response was,the more serious immunity suppression was.The damages of SIRS to CPB were the result of inflammatory response and anti-inflammmatory response .It was a new idea when treating SIRS that the pro-inflammatory cytokines were resisted and immunity function was improved,at the same time to reach the balance between pro-inflammatory and anti-inflammatory cytokines.
关 键 词:体外循环 单核细胞HLA-DR 炎症反应 抗炎反应 免疫抑制
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