羟乙基淀粉130/0.4改善大鼠心肌缺血再灌注损伤
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军队“十一五”科技攻关项目(08G071).


Protective effects of hydroxyethyl starch 130/0.4 against myocardial ischemia-reperfusion injury in rats
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Supported by the “11th Five-Year Plan” for Scientific and Technological Project of PLA(08G071).

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    摘要:

    目的:观察羟乙基淀粉(HES)130/0.4(万汶)对缺血再灌注(I/R)损伤心肌的干预作用,探讨其可能的作用机制。方法:24只SD大鼠随机均分为4组(n=6):假手术(S)组、缺血再灌注(IR)组、白蛋白-缺血再灌注(A-IR)组、HES-缺血再灌注(H-IR)组。后3组建立在体大鼠心肌I/R模型,分别在缺血25 min时股静脉持续泵入生理盐水、5%白蛋白或HES 130/0.4,假手术组行开胸手术但不结扎左冠状动脉前降支。再灌注180 min处死大鼠,取心肌组织观察病理学改变;处死前颈动脉采血ELISA法测定TNF-α、IL-1β浓度;测定心肌组织NF-κB活性。结果:H-IR组心肌组织损伤病理学改变较IR组、A-IR组减轻。IR组、A-IR组、H-IR组血清TNF-α、IL-1β水平和心肌NF-κB活性明显高于S组(P<0.05),但其中H-IR组血清TNF-α、IL-1β水平及心肌NF-κB活性上升程度不及IR组、A-IR组(P<0.05)。结论:羟乙基淀粉130/0.4能减轻缺血再灌注所致心肌病理损伤,可能与其抑制NF-κB的活性、减少促炎细胞因子的释放有关。

    Abstract:

    Objective:To explore the influence of hydroxyethyl starch(HES) 130/0.4 on myocardial ischemia-reperfusion (I/R) injury in rats and the possible mechanism.Methods: Twenty-four SD rats were evenly randomized into four groups(n=6):the sham operation group,the I/R(IR) group,albumin + I/R(A-IR) group,and HES+I/R(H-IR) group; rats in the latter three groups were made into I/R models and were treated respectively with 7.5 ml/kg saline,5% albumin and HES 130/0.4 through femoral vein at 25 min of ischemia.At 180 min of reperfusion,animals were sacrificed and the pathological changes of myocardium were observed.Serum concentrations of TNF-α and IL-1β and the myocardial NF-κB activity were also measured.Results: Histological examination showed that the injury in H-IR group was ameliorated compared with those in IR and A-IR groups.NF-κB activity and TNF-α ,IL-1β concentrations in the sham operation group were significantly lower than those of the other 3 groups (P<0.05); and the increases of the above parameters in H-IR group were smaller than those of the IR and A-IR groups (P<0.05).Conclusion: HES 130/0.4 can improve myocardial function and attenuate ischemia-reperfusion injury,and the mechanism might be related to the inhibition of myocardial NF-κB activity and reduction of proinflammatory factors.

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  • 收稿日期:2009-02-24
  • 最后修改日期:2009-06-01
  • 录用日期:2009-07-21
  • 在线发布日期: 2009-08-25
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