期刊文献+

亚低温在大鼠脑缺血再灌注中的脑保护作用 被引量:3

The protective effect of mild hypothermia in cerebral ischemia and reperfusion in rats
原文传递
导出
摘要 目的探讨亚低温在脑缺血再灌注损伤中的保护作用。方法采用大鼠大脑中动脉线栓闭塞/再通法建立大鼠局灶性缺血-再灌注模型,常温组和亚低温组分别于脑缺血3 h再灌注6 h、12 h、24 h、 48 h、72 h后断头取脑,假手术组则于再灌注24 h断头取脑,测定MPO的活性和免疫组化法观察ICAM-1、 Mac-1的表达,同时常温组和亚低温组在再灌注24 h进行神经功能评分和脑梗死体积的比较。结果 (1)脑缺血再灌注6 h后,脑缺血灶ICAM-1和Mac-1表达逐渐出现增高趋势,脑组织MPO活性也逐步增高,再灌注 48 h达高峰,它们与假手术组比较差异有统计学意义(P<0.05,P<0.01)。(2)缺血早期进行亚低温干预,能明显抑制ICAM-1、Mac-1的表达和MPO活性(P<0.05,P<0.01)。(3)亚低温可以改善大鼠脑缺血再灌注后的神经功能障碍,减少脑梗死体积(P<0.01)。结论脑缺血再灌注后炎症反应是造成脑损伤的重要因素之一;亚低温干预能明显抑制再灌注后脑组织炎症反应,起到神经保护作用,这可能是亚低温在脑缺血再灌注损伤中的重要保护机制之一。 Objective To investigate the protective effect of mild hypothermia during cerebral ischemia and reperfusion. Methods After 3 hours of middle cerebral artery occlusion (MCAO) in rats, the myeloperoxidase (MPO) activity, the positive expression of intercellular adhesion molecule-1 (ICAM-1) , and the leukocyte integrin Mac-1 ( CD11 b/CD18 ) level in the ischemic regions were determined at different times ( 6 h, 12 h ,24 h, 48 h and 72 h) during and after 24 h of reperfusion. Cerebral infarction volume and neurological function were also evaluated in a control group, in addition to the above variables, at 24 hours of reperfusion. Results The MPO activity and the expression of ICAM-1 and Mac-1 were significantly elevated at 6 h after cerebral ischemia during reperfusion. These variables peaked at 48 h. There was a remarkable difference between the various groups and a sham-operated group ( P 〈 0.05, P 〈 0.01 ). Mild hypothermia reduced M PO activity and the positive expression of ICAM-1 and Mac-1 in brain tissue ( P 〈 0.05 ,P 〈 0.01 ). Conclusion Mild hypothermia can ameliorate any neurological deficit and decrease the infarct volume induced by cerebral ischemia and reperfusion. During cerebral isehemia-reperfusion, mild hypothermia could play an important role in decreasing the early onset of any inflammatory cascade reaction, which might be one of the neuroprotcetive mechanisms of mild hypothermia.
出处 《中华物理医学与康复杂志》 CAS CSCD 北大核心 2006年第3期158-161,共4页 Chinese Journal of Physical Medicine and Rehabilitation
关键词 亚低温 脑缺血 再灌注损伤 细胞间粘附分子 髓过氧化物酶 Mild hypothermia Cerebral ischemia-reperfusion Intercellular adhesion molecule-1 Myeloperoxidase
  • 相关文献

参考文献10

二级参考文献49

  • 1Barone FC, Feuerstein GZ. Inflammatory mediators and stroke:new opportunities for novel therapeutics. J Cereb Blood Flow Metab, 1999,19:819.
  • 2Yang GY, Mao Y, Zhou LF, et al.Expression of intercellular adhesion 1 (ICAM-1) is reduced in permanent focal cerebral ischemic mouse brain using an adenoviral vector to induce overexpression of interleukin-1 receptor antagonist. Brain Res Mol,1999,65:143.
  • 3Barone FC, Arvin B, White RF, et al. Tumor necrosis factor-α: a mediator of facal ischemic brain injury. Stroke, 1997,28:1233.
  • 4Zhang WD, Fmith C, Shapiro A, et al.Increased expression of bioactive chemokines in human cerebromicrovascular endothelial cells and astrocytes subjected to simulated ischemia in vitro.J Neuroimmunol,1999,101:148
  • 5Stoll G,Jander S,Schroeter M. Inflammation and glial responses in ischemic brain lesions. Prog Neurobiol, 1998,56 : 149.
  • 6Prestigiacomo CJ,Kim SC,Connolly ES,et al. CD18-mediated neutrophil recruitment contributes to the pathogenesis of reperfused but not nonreperfused stroke. Stroke, 1999,30:1110.
  • 7Ward PA. Mechanisms of endothelial cell killing by H2O2 or products of activated neutrophils. Am J Med, 1991,91:89.
  • 8Kawai N, Okauchi M, Morisaki K, et al. Effects of ddlayed intraischemic and postischemic hypothermia on a focal model of transient cerebral ischemia in rats. Stroke ,2000,31 : 1982.
  • 9Gregersen R,Lambertsen K,Finsen B. Microglia and macrophages are the major source of tumor necrosis factor in permanent middle cerebral artery occlusion in mice. J Cereb Blood Flow Metab,2000,20:53.
  • 10Maier CM, Ahern K, Cheng ML,et al. Optimal depth and duration of hypothermia in a focal model of transient cerebral ischemia: effects on neurologic outcome, infarctsize, apoptosis, and inflammation. Stroke, 1998,29:2171-2180.

共引文献38

同被引文献44

引证文献3

二级引证文献7

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