简介：目的研究HIF-1对大鼠急性缺血心肌的保护作用及其作用机制。方法应用HIF-1活性诱导剂氯化钴预处理大鼠,观察预处理对大鼠急性心肌梗死面积和心肌VEGF、iNOS蛋白表达的影响。结果氯化钴预处理组大鼠较对照组和假手术组急性心肌梗死面积显著减少（P〈0.01）,VEGF、iNOS蛋白表达显著增高（P〈0.01）。结论HIF-1可以减少大鼠急性心肌梗死面积,对大鼠急性缺血心肌具有保护作用,其机制可能与HIF-1促进VEGF、iNOS蛋白表达增加有关。

简介：ObjectivesTostudyclinicalandcoronaryangiographicfindingsinpatientswithbothcoronaryheartdiseases(CHD)andtype2diabetesmellitus(T2DM).Methods215patientswithCHDconfirmedbycoronaryangiographywereinvolvedinthisstudy.Thepatientsweredividedintotwogroups:74CHDpatientswithT2DM(meanage64.7±8.2years,male/female47/27),and141CHDpatientswithoutT2DM(meanage66.2±9.2years,male/female100/41).Theclinicalfeaturesandthedatafromselectivecoronaryangiographieswerecomparedbetweentype2diabeticandnon-diabeticCHDpatients.ResultsComparedtonon-diabeticCHDpatients,thepatientswithbothCHDandT2DMsufferedmorefromacutemyocardialinfarction,silentischemiaandseverearrhythmias(P＜0.01,P＜0.05),andhadhigherserumtriglyceridesandapo-lipoproteinB,alongwithincreasedserumuricacid(P＜0.01,P＜0.05),increasedleftventricularenddiastolicdiameter(P＜0.01),anddecreasedleftventricularejectionfraction(P＜0.001).Comparedtonon-diabeticCHDpatients,thepatientswithbothCHDandT2DMsufferedmorefromtriplevesseldisease(P＜0.01),severecoronaryarterystenosis,completeocclusionsanddiffuselesions(P＜0.001).ConclusionsSevereclinicalmanifestation,leftventriculardysfunction,diffuseorcomplicatedlesionsofcoronaryarteriesweremorecommoninpatientswithbothCHDandT2DM,itsuggeststhatthetype2diabeticCHDpatientshavepoorprognosis.

简介：Themyocardialprotectionaffordedbyischemicpreconditioning(IPC)canalleviateischemia-reperfusioninjuryinnormalratheart.However,thismyocardialprotectionisseldomstudiedinthetype2diabeticratwithmyocardialischemiadisease.Inthisstudy,weaimedtoevaluatetheeffectsofATP-sensitivepotassiumchannels(KATPchannels)onIPCintheisolatedtype2diabeticratheartandtheroleofthesulfonylureagliclazide.MethodsStreptozotocin(STZ)-inducedtype2diabeticmaleWistarratswithorwithoutgliclazide(64mg/kgbodyweight,orally)andage-matchednon-diabeticcontrolratswereusedforallstudies.TheisolatedheartswereperfusedwithLangendorff'ssystemundertheconstantflow,pressureandtemperatureconditionswithKreb's-Henseleitsolution(K-H).After5minutesofbalanceperfusion,theseratswererandomlydividedintosixgroups:non-diabeticcontrolratswithoutIPC(CIR);non-diabeticcontrolratswithIPC(CIP);diabeticratswithoutIPC(DIR);diabeticratswithIPC(DIP);gliclazide-treateddiabeticratswithoutIPC(GIR);andgliclazide-treateddiabeticratswithIPC(GIP).GroupsCIR,DIR,andGIRweresubjectedto30-minglobalischemiaand60-minreperfusionforinductionofischemia/reperfusioninjury.GroupsCIP,DIP,andGIPweregiventhreecyclesof5-minischemiaand5-minreperfusionasIPC,andthenischemia/reperfusioninjuryprogramwasimplemented.Extentofischemia/reperfusioninjurywasmeasuredintermsofthereleaseoflactatedehydrogenase(LDH),creatinekinase(CK),andcreatinkinase-MB(CKMB)incoronaryeffluent.Afterperfusion,Kir6.2andSUR2AmRNAexpressionsinthemyocardialtissuewerecharacterizedbyfluorescentquantitativereal-timePCRmethod,andKir6.2andSUR2Aproteinexpressionswereassessedbyimmunohistochemistry.ResultInnon-diabeticcontrolrats,thereleaseofLDH,CK,andCK-MBincoronaryeffluentmarkedlydecreasedwithIPCcomparedwithNo-IPC(P<0.05),butnotindiabeticrats.However,ingliclazide-treateddiabeticrats,IPC-induceddecreaseintherele

简介：ObjectivesTheeffectsofcarvediloloncalciumcurrent(ICa)wereinvestigatedinisolatedadultratventricularmyocytes.MethodsICawasrecordedbyusingwhole-cellpatch-clamprecordingtechnique.ResultsCarvedilolreversiblyinhibitedICainaconcentration-dependentmanner,carvedilolat0.1,0.3,1and10μmol/LintheextracellularsolutiondecreasedpeakICaby1.52%,18.04%,37.34%and72.18%,respectively.Thesteady-stateinactivationcurveofICawasshiftedtomorenegativepotentials,whiletheactivationcurvewasnotaltered.Therecoveryfrominactivationwasshiftedtorightdirection,itcouldnotberecoveredcompletely.Inaddition,Pretreatmentofventricularmyocyteswithprazosinandpropranololcouldn'tblockthecarvedilol-inducedreductionofICa.ConclusionsCarvedilolinhibitsICainadultratventricularmyocytesbymechanismsinvolvingpreferentialinteractionwiththeinactivatedstateofcalciumchannel.

简介：目的：探讨2型糖尿病（T2DM）合并高血压与否对脂代谢、微血管病变、血液流变学的影响。方法：192例T2DM患者被分为血压正常组（A组，96例）和合并高血压组（B组，100例），对两组的一般情况、血压、脂代谢、微血管损害及血液流变学情况进行比较分析。结果：B组的血压（148±24）mmHg／（86±15）mmHg、胆固醇（6．0±0．9）mmol／L、血肌酐（70±21．1）μmol／L、血尿酸（343±81）μmol／L和低切粘度（11．02±2．3）均高于A组，有显著性差异（P〈0．05-〈0．01）。结论：T2DM和高血压病均可导致血脂代谢异常，微血管损害和血液流变学的改变，当T2DM合并高血压时，前述异常和损害加重，应及早控制。

简介：目的对中西医结合治疗在2型糖尿病患者中的治疗方式进行讨论。方法选取我院2013年2月-2014年2月间64例2型糖尿病患者,将其分为两组,1组进行常规治疗,2组在进行常规治疗的同时配合中药治疗,对两组患者的治疗效果进行比较。结果1组患者治疗后效果显著的为13例,占比例的40.6%,治疗有效的为14例,占比例的43.8%,治疗无效的患者为5例,占比例的15.6%。2组患者治疗效果显著的为23例,占比例的71.9%,治疗有效的为8例,占比例的25%,治疗无效的仅为1例,占比例的3.1%。结论中西医结合方式治疗2型糖尿病的效果显著,且安全性高,是一种值得推广的治疗方式。

简介：目的总结2例新生儿动脉导管支架植入术的护理经验.方法完善术前检查,用药护理,生命体征的观察,血氧饱和度的监测,尽早采取介入手术方法.术后密切监测生命体征,伤口渗血情况,尿色,足背动脉搏动情况,肢温情况,及时发现并处理并发症.结果病例1术后2个月院外死亡,考虑死亡原因为动脉导管支架再狭窄后的低氧血症.病例2半年后顺利进行2期外科手术.结论术后密切监测生命体征的变化,特别是血氧饱和度,及时发现并处理并发症是新生儿动脉导管支架植入术护理的关键.

简介：动脉粥样硬化（AS）是一种炎症性疾病，脂蛋白相关磷脂酶A2（lipoprotein-associatedphospholipaseA2，Lp-PLA2）是心血管疾病中一种新的炎症酶，能水解氧化低密度脂蛋白（LDL），产生溶血磷脂酰胆碱（lysophosphatidyl-choline，Lyso-PC）和氧化型游离脂肪酸（oxidizedfreefat-tyacids，ox-FA），促进动脉粥样硬化的形成和发展，其与临床疾病的关系日益受到关注。

简介：摘要目的探究对2型糖尿病患者实施延续护理的临床效果。方法将64例2型糖尿病患者作为研究对象，并随机将其分为对照组和观察组，给予对照组常规门诊护理，观察组在对照组基础上加用延续护理，对两组患者护理后的依从性进行评估。结果观察组32例患者饮食控制、运动疗法、饮食控制、自我检测状况明显要比对照组患者高，对比差异具有统计学意义（P＜0.05）。结论对2型糖尿病患者采用延续护理，能够明显提高病人的治疗依从性，提高患者的生活质量，在临床上值得大力推广。

简介：ObjectivesToevaluateantihypertensiveefficiencyandsafetyofanewdomesticofL-&N-typeCa^2+antagonist-eilnidipinewithimidaprilasapositivecontrol.MethodsAfter2weeks'placebowashingout,22patientsweretreatedwitheilnidipine5mgdailyand27patientsweretreatedwithimidapril5mgdaily.4weekslater,ifpatient'ssittingdiastolicbloodpressureisover90mmHg,his/herdosagewasdoubledforanother4weeks,theothersmeasuringupremainedtheirdosageunchangedforanother4weeks.Bloodpressure,heartrate,bloodandurineroutineexamination,serumglucose,serumchemicalexaminationincludingtotalcholesterol,triglyceride,HDL,LDL,transaminase,creatineetcandsidereactionswererecordedbeforeandafterthetrial.Datawereanalyzedstatistically.ResultsAfter8weeks'treatment,bloodpressurewassignificantlydecreased(P<0.05)inbothgroups,andthetwomedicineshadsimilarantihypertensiveeffects.Furthermore,thereducingofheartratewasstatisticallysignificantcomparedwithbaseline(P<0.01)inthecilnidipinegroup,butnotintheimidaprilgroup.Thenegativechronotropiceffectofcilnidipinehadlittleeffectoncontinuingthetherapy.Therewerenochangesonbloodandurineroutineexaminationandserumlipid,serumglucose,creatine,transaminaseandetcinbothgroups.Theirsidereactionsweremildandwell-tolerated.ConclusionsCilnidipinehasacon-vincingantihypertensiveeffectsimilartothatofimi-dapril.Especiallycilnidipinemaybeadministeredtopatientswithrelativelymildtachycardia.

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简介：患者男性，41岁。因腹痛、腹泻2小时就诊。体检：135／90mmHg，P55次／分，急性痛苦面容，脱水征不明显，双肺呼吸音清，心音有力，心律齐，未闻及病理性杂音。腹平软，脐周压痛（＋），无反跳痛，未触及包块，肝脾未触及，肠鸣音亢进，血常规：HB130g／L，WBC13．2×10^9／L，N0.78,L0．22。尿常规（-），大便常规示粘液便，细胞（＋），脓细胞（＋），潜血试验（-），血生化检查正常，大便培养（-）。ECG

简介：患者男性,59岁。因＂口干、多饮多尿1年,昏迷2小时余＂入院。既往有＂高血压＂病史10年,发现＂糖尿病＂1年。入院时查体：神志不清,烦躁,血压测不到,呼吸急促,两肺呼吸音粗,可闻及干啰音,心率90次/分,心律不齐,心音弱,

简介：患者男性，37岁。因突感心悸、心慌，急诊心电图（图1A）示：未见明显P波，心室率190次／分，QRS波群宽大畸形，呈完全性左束支传导阻滞形，R—R间距规整。aVL导联呈R形。心电图诊断：阵发性室性心动过速。彩超检查符合致心律失常性右室发育不良改变，经射频消融治疗后复查心电图（图1B）示：窦性心律，心率68次／分。右胸导联、下壁导联QRS波后可见一界限分明的低振幅小棘波（称Epsilon波），导致QRS波群酷似右束支阻滞形。

简介：目的观察脑出血后LINGO-1表达的变化,探讨维甲酸对脑出血后LINGO-1表达的影响。方法将72只SD大鼠随机分为假手术组、模型组和维甲酸治疗组,选取造模后1d、3d、7d和14d为观察点。制备脑出血模型,Longa评分法评价神经功能缺损程度,RT-PCR法检测LINGO-1mRNA的表达,Westernblot法检测LINGO-1蛋白的表达。结果模型组Longa评分7d最高,14d出现下降;LONG-1mRNA3d表达最高,7-14d出现下降;LONG-1蛋白7d到高峰,14d出现下降。维甲酸治疗组在14dLonga评分较模型组下降（P〈0.05）;在7d和14dLINGO-1mRNA表达较模型组下降（P〈0.05）;在14dLINGO-1蛋白表达较模型组下降（P〈0.05）。结论脑出血后LINGO-1表达明显上调,呈先上升后下降的变化规律。维甲酸可以降低LINGO-1mRNA和蛋白的表达及神经功能评分。

简介：患者女性，14岁。于入院前12h在劳动时突发胸骨后持续性疼痛，伴心慌、气短、咳嗽、咯粉红色泡沫样痰，急诊入院。查体：血压80／50mmHg，大汗淋漓，呼吸困难，121唇发绀，两肺可闻及广泛湿性哕音，心率140次／分，律齐，心音低钝，未闻及病理性杂音。心电图（图1A）示：窦性心律，心室率140次／分，Ⅰ、aVL导联呈qr型，q／r≥1，q波时限0．04s，V2-V6导联呈QS型，ST段呈弓背型抬高0．1～0．3mV，肢体导联QRS波群电压〈0．5mV，T波低平，心电图诊断：

简介：通常膜周部室间隔缺损的形态大致可分为4种类型,即漏斗型、窗型、管型和囊袋型(膜部瘤型)。从病理上室间隔膜部瘤分为真性和假性两种,真性室间隔膜部瘤是心脏膜部间隔向右侧心腔囊袋状突起的一种先天性畸形。而膜部瘤型室间隔缺损是室间隔缺损愈合过程中形成的,由于

简介：

简介：Thestudyaimedtoinvestigatetheeffectsofivabradineonthelevelsofhypoxia-induciblefactor-1alpha(HIF-1α)andVEGFinserumofrabbitwithacutemyocardialinfarction(AMI).MethodsAMImodelwasestablishedbyligatingtheleftanteriordescendingbranchofthecoronaryarteryinNewZealandwhiterabbits.Twentyfiverabbitswererandomlydividedinto4groups:sham-operated(S),myocardial-infarction(M)withbisoprololtreatment(M+B)andivabradine-treated(I+M).Themedicaltreatmentbeganimmediatelyafterinfarctionandcontinuedfor3weeks.Serumofeachrabbitwasobtainedatthefollowingtimepoints(24hbeforetheoperation,24h,3d,1week,2weeksand3weeksaftertheoperation).ELISAwasusedtomeasurethelevelsofHIF-1αandVEGFofeachsample.ECGandheartrates(beforeandaftertreatment)wereanalyzed.ResultsBaselineheartrateshowednosignificantdifferencesbetweenthe3infarctedgroups(M,M+B,M+I).ThreeweekslatertheheartratesweresignificantlyloweringroupM+BandgroupM+IthaningroupM.However,therewasnostatisticdifferencebetweenthetwodrug-treatedgroups(P=0.848).ThelevelsofHIF-1αandVEGFingroupsM,M+BandM+I)increasedsignificantlycomparedwithgroupS(P<0.01).TheproductionsofHIF-1αandVEGFwereloweringroupM+BandgroupM+IcomparedwithgroupM(P<0.01).TherewasnostatisticaldifferencebetweenthegroupM+BandgroupM+I(P>0.05),andthecorrelativeanalysisrevealedthattheproductionofHIF-1αwaspositivelycorrelatedwiththatofVEGF(r=0.732,P<0.01).ConclusionIvabradinecanreduceheartrateandmeanwhiledecreasetheserumlevelsofHIF-1αandVEGFafterAMI.

简介：患者男性，59岁。因活动后气短憋气7年，加重7天入院。查体：体温36．4℃，脉搏115次／分，呼吸28次／分，血压90／60mmHg。双肺听诊呼吸音清，未闻及干湿性啰音，心律75次／分，律齐，心音强弱不等，心尖部可闻及收缩期Ⅱ／Ⅵ级吹风样杂音，肺动脉瓣听诊区可闻及收缩期Ⅱ／Ⅵ级舒张期杂音，三尖瓣听诊区可闻及舒张期隆隆样杂音。查超声心动图示：肺栓塞，三尖瓣大量返流。肺动脉压约100mmHg，右心功能减低。心电图记录于发病当天，