期刊文献+

急性心肌梗死患者血清炎症因子的动态变化及相互关系 被引量:15

Temporal changes and interaction of serum cytokines in patients with acute myocardial infarction undergoing primary percutaneous coronary intervention
原文传递
导出
摘要 目的 观察急性心肌梗死患者经皮冠状动脉介入(PCI)治疗前后血清炎症因子白细胞介素(IL)及单核细胞趋化蛋白1(MCP-1)的动态变化及其相关关系.方法 2008年6-12月连续收集北京大学第三医院心内科住院的急性ST段抬高型心肌梗死(STEMI)患者59例.采用双抗体夹心ELISA分别检测STEMI患者PCI术前即刻、术后4~6、12、24 h、7 d血清IL-6、IL-8、MCP-1及IL-10的水平,比较不同时间血清炎症因子水平的变化,并对其炎症因子水平的自然对数作相关分析.结果 PCI术后12 h血清IL-6、IL-8(中位数)水平均显著高于术前(IL-6:8.51 ng/L比6.76 ng/L,IL-8:4.67ng/L比2.95 ng/L,均P<0.05).在PCI术后4~6 h及12 h,MCP-1的水平均显著高于术前(35.04ng/L,34.24 ng/L比30.45 ng/L,均P<0.05);而IL-10的水平比术前均显著降低(18.15 ng/L,18.82ng/L比20.95 ng/L,均P<0.05).PCI术前IL-6及IL-10水平与入院时心功能Killip分级均具有显著相关性(IL-6:r=0.293,P<0.05;IL-10:r=-0.287,P<0.05),PCI术前IL-8水平与胸痛发作时间呈负相关(r=-0.299,P<0.05).心肌梗死的部位、射血分数与各种炎症因子的水平差异无统计学意义(P>0.05);在各时间点,血清IL-6、IL-8及MCP-1浓度之间呈显著正相关性(P<0.01),分别与IL-10的呈显著负相关性(P<0.01).结论 心肌缺血再灌注后致炎因子水平升高而抗炎因子水平降低,机体存在炎症/抗炎状态失衡. Objective To investigate the temporal changes of serum cytokines IL-6,IL-8,MCP-1 and IL-10 immediately before and after primary PCI ( percutaneous coronary intervention ) in patients with ST-segment elevation myocardial infarction ( STEMI ) and explore the interaction of these cytokines.Methods A total of 59 STEMI patients were recruited.And their serum concentrations of IL-6,IL-8,MCP-1 and IL-10 were measured by ELISA before primary PCI and 4 -6 hours,12 hours,24 hours and 7 days postintervention.For each cytokine,the level at each time-point post-PCI was compared to that at pre-PCI.Correlation coefficient test was used to analyze the interactions of these four cytokines.Results At 12 hours post-PCI,the median serum levels of IL-6 and IL-8 were higher than those before PCI ( IL-6:8.51 ng/L vs 6.76 ng/L,IL-8:4.67 ng/L vs 2.95 ng/L,both P 〈0.05).At 4 -6 hours and 12 hours post-PCI,the median values of MCP-1 were increasing significantly compared to those at pre-PCI ( 35.04 ng/L,34.24 ng/L vs 30.45 ng/L,both P 〈0.05 ) while those of IL-10 decreased ( 18.15 ng/L,18.82 ng/L vs 20.95ng/L,both P 〈0.05).The levels of IL-6 and IL-10 at pre-PCI were associated with the Killip classification on admission ( 1L-6:r = 0.293,P 〈 0.05; IL-10:r = - 0.287,both P 〈 0.05 ).Except for IL-8,other cytokines had no significant relation with the time length from onset to admission (P 〉 0.05 ).Additionally,these four cytokines were not found to be related with the location and extension of myocardial infarction,ejection fraction and NT-proBNP.At each time-point,there were a positive relationship among the natural logarithms of the concentrations of IL-6,IL-8 and MCP-1 ( P 〈 0.01 ),all of which were inverse to the natural logarithm of the concentration of IL-10 (P 〈 0.01 ).Conclusions The pro-inflammatory cytokines increase while the anti-inflammatory cytokines decrease after myocardial ischemia/reperfusion.An imbalance of inflammatory cytokines may be present.
出处 《中华医学杂志》 CAS CSCD 北大核心 2011年第12期819-823,共5页 National Medical Journal of China
基金 国家重点基础研究发展计划"973"项目(2007CB512107)
关键词 心肌梗死 白细胞介素类 趋化因子 心肌再灌注 Myocardial infarction Interleukins Chemotactic factors Myocardial reperfusion
  • 相关文献

参考文献28

  • 1Entman ML,Smith CW.Postreperfusion inflammation:a model for reaction to injury in cardiovascular disease.Cardiovasc Res,1994,28:1301-1311.
  • 2Frangogiannis NG,Youker KA,Rossen RD,et al.Cytokines and the microcirculation in ischemia and reperfusion.J Mol Cell Cardiol,1998,30:2567-2576.
  • 3Frangogiannis Ng E M.Role of inflammation following myocardial ischemia and reperfusion.Dordrecht:Kluwer Academic,1997:569-584.
  • 4Mehta JL,Li DY.Inflammation in ischemic heart disease:response to tissue injury or a pathogenetic villain? Cardiovasc Res,1999,43:291-299.
  • 5Ito T,Ikeda U.Inflammatory cytokines and cardiovascular disease.Curr Drug Targets Inflamm Allergy,2003,2:257-265.
  • 6Ren G,Dewald O,Frangogiannis NG.Inflammatory mechanisms in myocardial infarction.Curr Drug Targets Inflamm Allergy,2003,2:242 -256.
  • 7Frangogiannis NG,Smith CW,Entman ML.The inflammatory response in myocardial infarction.Cardiovasc Res,2002,53:31-47.
  • 8Ikeda U,Ohkawa F,Seino Y,et al.Serum interleukin 6 levels become elevated in acute myocardial infarction.J Mol Cell Cardiol,1992,24:579-584.
  • 9Neumann FJ,Ott I,Gawaz M,et al.Cardiac release of cytokines and inflammatory responses in acute myocardial infarction.Circulation,1995,92:748-755.
  • 10李拥军,丁文惠,史力斌,高炜,洪涛,霍勇.急性心肌梗死急诊介入治疗对炎性细胞因子影响的研究[J].中华老年心脑血管病杂志,2006,8(4):231-233. 被引量:6

二级参考文献35

  • 1急性心肌梗塞溶栓疗法参考方案(1996年7月修订)[J].中华心血管病杂志,1996,24(5):328-329. 被引量:1319
  • 2[1]Ross R.Atherosclerosis:an inflammatory disease[J].N Engl J Med,1999,340:115.
  • 3[2]Okamura H,Tsutsi H,Komatsu T,et al.Cloning of a new cytokine that induces IFN-γ production by T cell[J].Nature,1995,378:88.
  • 4[3]Bazan JF,Timans JC,Kastelein RA.A newly defined interleukin-1[J]?Nature,1996,375:591.
  • 5[4]Okamura H,Tsutsui H,Kashiwamura S,et al.Interleukin-18:a novel cytokine that augments both innate and acquired immunity[J].Adv Immunol,1998,70:281.
  • 6[5]Dinarello CA.Interleukin-18,a proinflammatory cytokine[J].Eur Cytokine Netw,2000,11:483.
  • 7[6]Stewart CW,Punnaivanam R,Alan D.Interleukin-18 enhances atherosclerosis in apolipoprotein E-/- mice through release of interferon-γ[J].Circ Res,2002,90:e34.
  • 8[7]Norbert G,Galina K,Sukhova,Peter L,et al.Expression of Interleukin(IL)-18 and functional IL-18 receptor on human vascular endothelial cells,smooth muscle cells,and macrophages:implications for atherogenesis[J].Circulation,2000,18:11.
  • 9[8]Zial M,Anne C,Alexandra S,et al.Expression of Interleukin-18 in human atherosclerotic plaques and relation to plaque instability[J].Circulation,2001,104:1598.
  • 10[9]Zial M,Anne C,Alexandra S,et al.Interleukin-18/Interleukin-18 binding protein signaling modulates atherosclerotic lesion development and stability[J].Circ Res,2001,89:e41.

共引文献56

同被引文献146

引证文献15

二级引证文献89

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部