瑞芬太尼预处理对大鼠心肌缺血再灌注损伤保护作用的研究(1)
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【中图分类号】R969.4【文献标识码】A【文章编号】1185-1672(2009)-12-1074-04
【摘要】目的研究不同浓度瑞芬太尼对MIR大鼠心肌缺血再灌注时MIR心肌保护作用的可能机制。方法40只SD大鼠随机分为5组。对照组;模型组(缺血再灌注组);瑞芬太尼预处理各组:(瑞芬Ⅰ组浓度3μg•kg-1•min-1,瑞芬Ⅱ组浓度6μg•kg-1•min-1瑞芬Ⅲ组浓度为12μg•kg-1•min-1)。测心肌匀浆中心肌细胞膜Na+-K+-ATP酶和Ca2+-Mg2+-ATP酶活性、光镜观察心肌组织形态学变化;其中对照组、模型组、瑞芬Ⅱ组应用信号转导基因芯片技术检测心肌细胞凋亡相关基因表达。结果
与对照组比较,MIR时心肌细胞膜Na+-K+-ATP和Ca2+-Mg2+-ATP酶活性降低,心肌组织结构明显损伤,心律失常发生率上升;瑞芬太尼组呈剂量依赖性的提高心肌细胞膜上的Na+-K+-ATP酶和Ca2+-Mg2+-ATP酶的活性,减轻心肌组织结构损伤,减少再灌注性心律失常的发生。与对照组比较,MIR时Bax、Bcl-2、Bcl-2L1调亡相关基因表达下调,Bcl-2/Bax比率下降;瑞芬太尼组与MIR组比较,Bax、Bcl-2、表达上升而Bcl2a1、Bcl-2L1基因表达下降,同时Bcl-2/Bax比率升高。结论
瑞芬太尼预处理对在体MIR大鼠心肌有保护作用,其可能机制是恢复心肌细胞膜上的Na+-K+-ATP酶和Ca2+-Mg2+-ATP酶的活性、通过上调凋亡调控基因BCL-2/Bax比率,抑制心肌细胞凋亡而减轻心肌细胞损伤。
【关键词】瑞芬太尼;缺血再灌注损伤;基因芯片;基因表达
Remifentanilpretreatmentonmyocardialischemia-reperfusioninjuryprotectiveeffectof
HanLei,LiuZhaofang
Anesthesiology,ShanghaiFifthPeople'sHospital,200240,China
【Abstract】ObjectivetorevealtheprotectioneffectandthepossiblemechanismofremifentanilpretreatmenttoMIRrat.Methods
40maleSDratswererandomlydividedinto5groups:controlgroup,remifentanilpretreatmentgroup1,2,3(3,6or12μg.kg-1.min-1remifentanil)andMIRgroup.IntheMIRgrouptheratsweresubjectedto30minutesischemiafollowedby45minutesreperfusion.Intheremifentanilpretreatmentgroup1,2,3,theratsweregivenwith3,6or12μg.kg-1.min-1remifentanilbybeinginfusionedintovesselviafemoralveinfor15minutesbeforeischemia-reperfusionrespectively.Afterreperfusion,leftventricularmyocardiumsamplesofischemiaareawereimmediatelyprocessed,Na+/K+-ATPase,Ca2+-Mg2+ATPaseactivitiesweremeasured,andmyocardialhistomorphologywereobservedwithmicroscope.Atthesametime,expressionofrelatedapoptosisgeneweremeasuredwithgenearraytechnology,incontrolgroup,modelgroupandremifentanilpretreatmentgroup2.Results
Withtheadministrationofremifentaniltheincidenceofventriculararrhythmiaweresignificantlylowered.Comparedwiththecontrolgroup,theactivityofNa+-K+-ATPaseandCa2+-Mg2+-ATPaseincellmembranedecreasedremarkably,inMIRgroup.AndremifentanilpretreatmentcouldsignificantlyrestoretheactivityofNa+-K+-ATPaseandCa2+-Mg2+-ATPaseinadose-dependentmanner.Underlightmicroscopic,thereweremyocardialtissuepatchynecrosis,myocardialfiberbreakage,myocardialcelledemaandinflammatorycellfiltrationinMIRgroup.Comparedwiththecontrolgroup,intheMIRgroup,expressionofBax、Bcl-2、Bcl-2L1andBirc1bgenesweredepressed,andBcl-2/Baxratiodescended.AndcomparedwiththeMIRgroup,inremifentanilpreconditioninggroup2expressionofBax、Bcl-2、Birc1bgeneswereelevatedbutBcl2a1、Bcl-2L1weredepressed.WealsofoundBcl-2/Baxratioascended.Conclusion
RemifentanilpretreatmentcansignificantlyrestoretheactivityofNa+-K+-ATPaseandCa2+-Mg2+-ATPaseinadose-dependentmanner.RemifentanilcanprovideprotectionfortheheartofMIRratagainstischemiareperfusioninjurybyascendingBcl-2/Baxratio.
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