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时间:2018-08-31
《抑制心内直视术中核转录因子激活保护心肌.doc》由会员上传分享,免费在线阅读,更多相关内容在学术论文-天天文库。
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
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