抑制心内直视术中核转录因子激活保护心肌.doc

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1、抑制心内直视术中核转录因子激活保护心肌作者：王云，易定华，万荣华，顾绩伟，李军朋【关键词】心内直视手术；核转录因子；抑制；心肌　　摘要：目的在人类体外循环(CPB)心内直视手术中研究核转录因子kB(NFkB)的激活与心肌白细胞浸润及损伤的关系，并观察氧自由基清除剂辅酶Q10对NFkB激活的抑制作用及其对心肌的保护作用。方法选取47例接受CPB心内直视手术的成年患者，随机分为对照组30例，治疗组17例。治疗组手术前5d口服辅酶Q10片剂。在体外循环转机前、心脏缺血45min和再灌注45min时取右心房肌组织，做心肌组织病理学、超微结构及NFkB活性观察。术后观察血

2、流动力学指标、血管活性药物剂量和临床指标。结果在缺血45min及再灌注45min后，对照组心肌毛细血管腔内可见嗜中性白细胞聚集并黏附于内皮细胞，超微结构损害，细胞胞核和胞浆内均可见NFkB阳性表达；而治疗组心肌可见少数嗜中性细胞浸润，超微结构损害轻微，细胞胞核和胞浆内有微弱的NFkB阳性表达。术后两组血流动力学指标、血管活性药物剂量和临床指标间无显著差异。结论NFkB在心内直视术中的心肌缺血和再灌注病理过程中起重要作用，辅酶Q10对NFkB激活有明显抑制作用，并对心肌有保护作用。　　关键词：心内直视手术；核转录因子；抑制；心肌　　Protectingmyocar

3、diumbyinhibitingtheactivationof　nuclearfactorkappaBinopenheartsurgery　　ABSTRACT:ObjectiveToinvestigatetherelationshipoftheactivationofnuclearfactorkappaB(NFkB)withmyocardialneutrophilinfiltrationandinjuryinhumanopenheartsurgery,andtoobservetheinhibitingeffectontheactivationofNFkBandp

4、rotectingeffectonmyocardiumofthecoenzymeQ10,ascavengerofoxygenfreeradicals.MethodsFortysevenadultpatientsundergoingopenheartsurgerywererandomlydividedintotwogroups,thecontrolandthetreatment.CoenzymeQ10tabletsweregiventothetreatmentgroup5daysbeforeoperation.Biopsyofrightatriumformyoca

5、rdialpathology,activatedNFkBdetectionandultrastructureobservationweredonepriortocardiopulmonarybypass,45minutesofischemiaand45minutesofreperfusion.Thedynamicindexes,vasomotordrugdosage,andoutcomeswereobservedpostoperatively.ResultsUpon45minutesofischemiaand45minutesofreperfusion,inco

6、ntrolgrouptherewereneutrophilaccumulationandadhesionofvascularendothelium,ultrastructural5damages,andpositiveexpressionofNFkBbothinnucleiandcytoplasm,inmyocardium.Intreatmentgroup,therewereonlymildneutrophilinfiltrationandultrastructuraldamages,andweakpositiveexpressionofNFkBbothinnu

7、cleiandcytoplasm.However,thedynamicindexes,vasomotordrugdosage,andoutcomesoftwogroupswerenotsignificantlydifferent.ConclusionNFkBplaysanimportantroleinpathophysiologicalprocessofmyocardialischemiaandreperfusioninopenheartsurgery.CoenzymeQ10hasobviousinhibitingeffectonactivationofNFkB

8、andprotectin