2018
SUMOylation of VEGFR2 regulates its intracellular trafficking and pathological angiogenesis
Zhou HJ, Xu Z, Wang Z, Zhang H, Zhuang Z, Simons M, Min W. SUMOylation of VEGFR2 regulates its intracellular trafficking and pathological angiogenesis. Nature Communications 2018, 9: 3303. PMID: 30120232, PMCID: PMC6098000, DOI: 10.1038/s41467-018-05812-2.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCorneaCysteine EndopeptidasesDiabetes MellitusEndopeptidasesGene DeletionGene Knock-In TechniquesGene SilencingGolgi ApparatusHuman Umbilical Vein Endothelial CellsHumansIntracellular SpaceMaleMice, Inbred C57BLMice, KnockoutNeovascularization, PathologicProtein TransportRetinaSignal TransductionSUMO-1 ProteinSumoylationVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2ConceptsPathological angiogenesisPotential therapeutic targetRegulation of VEGFR2Non-sumoylated formEndothelial-specific deletionDiabetic miceHindlimb ischemiaTherapeutic targetDiabetic settingControl of angiogenesisEndothelial cellsAngiogenesisVEGFR2Surface expressionVEGFR2 activityTissue repairSENP1
2014
PTP1b Is a Physiologic Regulator of Vascular Endothelial Growth Factor Signaling in Endothelial Cells
Lanahan AA, Lech D, Dubrac A, Zhang J, Zhuang ZW, Eichmann A, Simons M. PTP1b Is a Physiologic Regulator of Vascular Endothelial Growth Factor Signaling in Endothelial Cells. Circulation 2014, 130: 902-909. PMID: 24982127, PMCID: PMC6060619, DOI: 10.1161/circulationaha.114.009683.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAortaCell MovementCell ProliferationDisease Models, AnimalEndothelial CellsFemaleHindlimbHuman Umbilical Vein Endothelial CellsIschemiaMaleMiceMice, Mutant StrainsNeovascularization, PhysiologicPrimary Cell CultureProtein Tyrosine Phosphatase, Non-Receptor Type 1RNA, Small InterferingSignal TransductionVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2ConceptsPhosphotyrosine phosphatase 1BVascular endothelial growth factor receptor 2 signalingExtracellular signal-regulated kinaseGrowth factor signalingVEGF-dependent activationSignal-regulated kinaseNull miceVascular endothelial growth factor signalingRegulation of angiogenesisEndothelial traffickingEndothelial-specific deletionFactor signalingEndothelial VEGFR2Phosphatase 1BEndothelial cellsKey regulatorReceptor 2 signalingVEGFR2 signalingSignalingImportant roleEndothelial knockoutPhysiologic regulatorHindlimb ischemia mouse modelRegulationImpaired blood flow recovery
2013
Endothelial ERK signaling controls lymphatic fate specification
Deng Y, Atri D, Eichmann A, Simons M. Endothelial ERK signaling controls lymphatic fate specification. Journal Of Clinical Investigation 2013, 123: 1202-1215. PMID: 23391722, PMCID: PMC3582116, DOI: 10.1172/jci63034.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAortaBody PatterningButadienesCells, CulturedEndothelium, LymphaticExtracellular Signal-Regulated MAP KinasesFemaleGene ExpressionGene Expression Regulation, DevelopmentalHomeodomain ProteinsHuman Umbilical Vein Endothelial CellsHumansLymphangiectasisLymphangiogenesisMaleMAP Kinase Signaling SystemMiceMice, TransgenicMutation, MissenseNitrilesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-rafSOXF Transcription FactorsTumor Suppressor ProteinsUp-RegulationVascular Endothelial Growth Factor Receptor-3ConceptsFate specificationERK activationSOX18 expressionEndothelial cellsLymphatic endothelial cellsInhibition of ERKLymphatic fateDifferentiation programNoonan syndromeLymphatic phenotypeInducible expressionRAF1 geneMolecular eventsFunction mutationsProx1 expressionVenous endothelial cellsCardinal veinERKExpressionLymphatic vesselsKey roleRelated diseasesSOX18ActivationExcessive production
2001
PR-39 and PR-11 peptides inhibit ischemia-reperfusion injury by blocking proteasome-mediated IκBα degradation
Bao J, Sato K, Li M, Gao Y, Abid R, Aird W, Simons M, Post M. PR-39 and PR-11 peptides inhibit ischemia-reperfusion injury by blocking proteasome-mediated IκBα degradation. AJP Heart And Circulatory Physiology 2001, 281: h2612-h2618. PMID: 11709430, DOI: 10.1152/ajpheart.2001.281.6.h2612.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnti-Bacterial AgentsAntimicrobial Cationic PeptidesCells, CulturedCysteine EndopeptidasesDNA-Binding ProteinsEndothelium, VascularHumansI-kappa B ProteinsIntercellular Adhesion Molecule-1MaleMultienzyme ComplexesMyocardial Reperfusion InjuryMyocardiumNADPH OxidasesNeutrophilsNF-KappaB Inhibitor alphaPeptide FragmentsPeroxidasePhosphoproteinsProteasome Endopeptidase ComplexRatsRats, Sprague-DawleyReactive Oxygen SpeciesUmbilical VeinsVascular Cell Adhesion Molecule-1Ventricular Function, LeftConceptsIschemia-reperfusion injuryB alpha degradationAdhesion molecule-1PR-11Alpha degradationNeutrophil infiltrationMyeloperoxidase activityInfarct sizeMolecule-1Vascular cell adhesion molecule-1Myocardial ischemia-reperfusion injuryIntercellular adhesion molecule-1Cell adhesion molecule-1Ventricular systolic pressureTime of reperfusionIschemia-reperfusion modelMin of ischemiaPR-39Controls 24 hBlood pressureSystolic pressureCardiac functionIntramyocardial injectionIκBα degradationAdhesion moleculesAn anti-CD11/CD18 monoclonal antibody in patients with acute myocardial infarction having percutaneous transluminal coronary angioplasty (the FESTIVAL study)
Rusnak J, Kopecky S, Clements I, Gibbons R, Holland A, Peterman H, Martin J, Saoud J, Feldman R, Breisblatt W, Simons M, Gessler C, Yu A, Investigators F. An anti-CD11/CD18 monoclonal antibody in patients with acute myocardial infarction having percutaneous transluminal coronary angioplasty (the FESTIVAL study). The American Journal Of Cardiology 2001, 88: 482-487. PMID: 11524054, DOI: 10.1016/s0002-9149(01)01723-4.Peer-Reviewed Original ResearchMeSH KeywordsAgedAngioplasty, Balloon, CoronaryAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedChi-Square DistributionCombined Modality TherapyCoronary AngiographyDose-Response Relationship, DrugDouble-Blind MethodDrug Administration ScheduleElectrocardiographyFemaleFollow-Up StudiesHumansInfusions, IntravenousMaleMiddle AgedMyocardial InfarctionNeuroprotective AgentsPilot ProjectsProbabilitySensitivity and SpecificitySeverity of Illness IndexStatistics, NonparametricSurvival RateTomography, Emission-Computed, Single-PhotonTreatment OutcomeConceptsPercutaneous transluminal coronary angioplastyAcute myocardial infarctionIntercellular adhesion molecule-1Hu23F2GTransluminal coronary angioplastyCD11/CD18Monoclonal antibodiesCoronary angioplastyMyocardial infarctionCD11/CD18 monoclonal antibodyMyocardial single photon emissionInitial clinical safetySubsequent cardiac interventionsST-segment elevationHumanized monoclonal antibodyActivation of neutrophilsAdhesion molecule-1CD18 monoclonal antibodySignificant differencesG treatment groupsNear-baseline valuesSingle photon emissionAdverse eventsCoronary reperfusionInflammatory mediatorsSerial Motion Assessment by Reference Tracking (SMART): Application to Detection of Local Functional Impact of Chronic Myocardial Ischemia
Pearlman J, Gertz Z, Wu Y, Simons M, Post M. Serial Motion Assessment by Reference Tracking (SMART): Application to Detection of Local Functional Impact of Chronic Myocardial Ischemia. Journal Of Computer Assisted Tomography 2001, 25: 558-562. PMID: 11473185, DOI: 10.1097/00004728-200107000-00008.Peer-Reviewed Original ResearchExpression of vascular endothelial growth factor and its receptors is increased, but microvascular relaxation is impaired in patients after acute myocardial ischemia
Xu X, Li J, Simons M, Li J, Laham R, Sellke F. Expression of vascular endothelial growth factor and its receptors is increased, but microvascular relaxation is impaired in patients after acute myocardial ischemia. Journal Of Thoracic And Cardiovascular Surgery 2001, 121: 735-742. PMID: 11279416, DOI: 10.1067/mtc.2001.112340.Peer-Reviewed Original ResearchMeSH KeywordsAcute DiseaseBiomarkersBlotting, WesternCoronary Artery BypassCoronary CirculationCoronary VesselsDNA ProbesEndothelial Growth FactorsEnzyme InhibitorsFemaleGene ExpressionHeart AtriaHumansLymphokinesMaleMiddle AgedMyocardial IschemiaNitroarginineNitroprussidePrognosisProtein IsoformsReceptor Protein-Tyrosine KinasesReceptor, Fibroblast Growth Factor, Type 1Receptors, Fibroblast Growth FactorReceptors, Growth FactorReceptors, MitogenReceptors, Vascular Endothelial Growth FactorReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSubstance PVascular Endothelial Growth Factor AVascular Endothelial Growth FactorsVasodilationVasodilator AgentsConceptsVascular endothelial growth factorEndothelial growth factorAcute myocardial ischemiaGrowth factor receptor 1Vascular endothelial growth factor receptor 1Vascular endothelial growth factor receptorFactor receptor 1Endothelial growth factor receptorMyocardial ischemiaGrowth factorReceptor 1Growth factor receptorMicrovascular relaxationFactor receptorGrowth factor receptor 2Protein expressionCoronary bypass operationsEndothelial growth factor receptor 2Vascular endothelial growth factor receptor 2Rat myocardial infarction modelFactor receptor 2Human atrial tissueVascular endothelial growthMyocardial infarction modelMessenger RNA levelsPharmacokinetics and Pharmacodynamics of Recombinant FGF‐2 in a Phase I Trial in Coronary Artery Disease
Bush M, Samara E, Whitehouse MJ, Yoshizawa C, Novicki D, Pike M, Laham R, Simons M, Chronos N. Pharmacokinetics and Pharmacodynamics of Recombinant FGF‐2 in a Phase I Trial in Coronary Artery Disease. The Journal Of Clinical Pharmacology 2001, 41: 378-385. PMID: 11304894, DOI: 10.1177/00912700122010230.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overArea Under CurveCoronary DiseaseEnzyme-Linked Immunosorbent AssayFemaleFibroblast Growth Factor 2Follow-Up StudiesHemodynamicsHeparinHumansInfusions, IntravenousMaleMaximum Tolerated DoseMetabolic Clearance RateMiddle AgedRecombinant ProteinsRegression AnalysisTime FactorsConceptsRecombinant FGF-2Coronary artery diseasePhase I trialFibroblast growth factor-2Artery diseaseI trialSystemic exposureSevere coronary artery diseaseTerminal elimination t1/2Peak plasma concentrationConcentration-time curveMultiple animal modelsDose-response relationshipAcute hemodynamicsGrowth factor 2Chronic ischemiaElimination t1/2Intravenous infusionSingle doseLinear pharmacokineticsDistribution t1/2Plasma concentrationsIntravenous administrationBiphasic eliminationSlow clearanceEfficacy of intracoronary or intravenous VEGF165 in a pig model of chronic myocardial ischemia
Sato K, Wu T, Laham R, Johnson R, Douglas P, Li J, Sellke F, Bunting S, Simons M, Post M. Efficacy of intracoronary or intravenous VEGF165 in a pig model of chronic myocardial ischemia. Journal Of The American College Of Cardiology 2001, 37: 616-623. PMID: 11216988, DOI: 10.1016/s0735-1097(00)01144-x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCoronary CirculationDose-Response Relationship, DrugEndothelial Growth FactorsEndothelium, VascularInfusions, Intra-ArterialInfusions, IntravenousLymphokinesMaleMicrocirculationMyocardial ContractionMyocardial IschemiaSwineVascular Endothelial Growth Factor AVascular Endothelial Growth FactorsConceptsChronic myocardial ischemiaMyocardial ischemiaL-NAMEIntracoronary groupBlood flowNitro-L-arginine methyl ester hydrochlorideNitric oxide synthase inhibitionEndothelial growth factor treatmentLeft circumflex coronary arteryDose-limiting hypotensionOxide synthase inhibitionCircumflex coronary arteryVascular endothelial growth factor treatmentMyocardial blood flowRegional myocardial functionGrowth factor treatmentVEGF-induced angiogenesisIntravenous groupConcomitant administrationMicrovascular functionIntracoronary infusionCollateral indexDifferent regimensCoronary arteryIntravenous infusionSerotonin-induced human coronary microvascular contraction during acute myocardial ischemia is blocked by COX-2 inhibition
Métais C, Bianchi C, Li J, Li J, Simons M, Sellke F. Serotonin-induced human coronary microvascular contraction during acute myocardial ischemia is blocked by COX-2 inhibition. Basic Research In Cardiology 2001, 96: 59-67. PMID: 11215533, DOI: 10.1007/s003950170078.Peer-Reviewed Original ResearchMeSH KeywordsAgedCoronary VesselsCyclooxygenase 1Cyclooxygenase 2Cyclooxygenase 2 InhibitorsCyclooxygenase InhibitorsFemaleHeart AtriaHumansIsoenzymesMaleMembrane ProteinsMicrocirculationMiddle AgedMyocardial IschemiaMyocardiumNitric Oxide SynthaseNitric Oxide Synthase Type IINitric Oxide Synthase Type IIINitroprussideProstaglandin-Endoperoxide SynthasesSerotoninSubstance PVasoconstrictionConceptsAcute myocardial ischemiaMyocardial ischemiaContractile responseCoronary arteriolesPotent contractile responseAcute coronary syndromeCOX-2 expressionCOX-2 inhibitionCOX-2 mRNAMicrovascular contractionSNP relaxationCoronary spasmCoronary syndromeL-NNACardiac surgeryAtherosclerotic patientsSubstance PNOS-2Prostaglandin releaseCOX-1IschemiaAtrial tissueSodium nitroprussideNOS-3Prostacyclin synthase
2000
Intracoronary basic fibroblast growth factor (FGF-2) in patients with severe ischemic heart disease: results of a Phase I open-label dose escalation study
Laham R, Chronos N, Pike M, Leimbach M, Udelson J, Pearlman J, Pettigrew R, Whitehouse MJ, Yoshizawa C, Simons M. Intracoronary basic fibroblast growth factor (FGF-2) in patients with severe ischemic heart disease: results of a Phase I open-label dose escalation study. Journal Of The American College Of Cardiology 2000, 36: 2132-2139. PMID: 11127452, DOI: 10.1016/s0735-1097(00)00988-8.Peer-Reviewed Original ResearchConceptsIntracoronary basic fibroblast growth factorOpen-label dose-escalation studyDose-escalation studyIschemic heart diseaseBasic fibroblast growth factorFibroblast growth factorHeart diseaseGrowth factorPhase I open-label dose-escalation studyFGF-2Non-Q-wave myocardial infarctionSevere ischemic heart diseaseSeattle Angina QuestionnaireTreadmill exercise testingQuality of lifeRegional wall thickeningMagnetic resonance imagingRFGF-2Angina QuestionnaireExercise toleranceRetinal examinationEscalation studyExercise testingIntracoronary administrationLaboratory parametersInhibition of ubiquitin-proteasome pathway–mediated IκBα degradation by a naturally occurring antibacterial peptide
Gao Y, Lecker S, Post M, Hietaranta A, Li J, Volk R, Li M, Sato K, Saluja A, Steer M, Goldberg A, Simons M. Inhibition of ubiquitin-proteasome pathway–mediated IκBα degradation by a naturally occurring antibacterial peptide. Journal Of Clinical Investigation 2000, 106: 439-448. PMID: 10930447, PMCID: PMC314329, DOI: 10.1172/jci9826.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnti-Infective AgentsAntimicrobial Cationic PeptidesCells, CulturedCysteine EndopeptidasesDNA-Binding ProteinsGene ExpressionHumansI-kappa B ProteinsMaleMiceMice, Inbred ICRMice, TransgenicMultienzyme ComplexesMyocardial InfarctionNF-kappa BNF-KappaB Inhibitor alphaPancreatitisPeptidesProteasome Endopeptidase ComplexSwineUbiquitinsConceptsDependent gene expressionGene expressionNF-kappa BUbiquitin-proteasome pathwayB alpha phosphorylationValosin-containing proteinB alpha degradationNF-kappa B inhibitor ICellular functionsTranscription factorsAlpha phosphorylationBiological processesInhibitor IAlpha 7 subunitSelective regulationProteasome activityB alphaAntibacterial peptidesOverall proteasome activityAlpha degradationNF-kappaBCell culturesIκBα degradationExpressionPeptidesBasic FGF reduces stunning via a NOS2-dependent pathway in coronary-perfused mouse hearts
Hampton T, Amende I, Fong J, Laubach V, Li J, Metais C, Simons M. Basic FGF reduces stunning via a NOS2-dependent pathway in coronary-perfused mouse hearts. AJP Heart And Circulatory Physiology 2000, 279: h260-h268. PMID: 10899065, DOI: 10.1152/ajpheart.2000.279.1.h260.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCalciumCoronary VesselsEnzyme InhibitorsFemaleFibroblast Growth Factor 2HeartIn Vitro TechniquesLysineMaleMiceMice, Inbred C57BLMice, KnockoutMyocardial IschemiaMyocardial ReperfusionMyocardial StunningNG-Nitroarginine Methyl EsterNitric Oxide SynthaseNitric Oxide Synthase Type IIRecombinant ProteinsConceptsFGF-2Mouse heartsBasic FGFIschemia-reperfusion injuryExpression of NOS2Onset of ischemiaInducible NO synthaseBasic fibroblast growth factorNitric oxide productionNO-selective electrodeFibroblast growth factorLV dysfunctionIschemic contractureVentricular functionLV recoveryNO synthaseIntracellular calciumProtective effectTransgenic heartsOxide productionIschemiaGrowth factorReperfusionSelective inhibitorVehicle control
1999
Serotonin-Induced Coronary Contraction Increases After Blood Cardioplegia-Reperfusion
Métais C, Li J, Li J, Simons M, Sellke F. Serotonin-Induced Coronary Contraction Increases After Blood Cardioplegia-Reperfusion. Circulation 1999, 100: ii-328-ii-334. PMID: 10567324, DOI: 10.1161/01.cir.100.suppl_2.ii-328.Peer-Reviewed Original ResearchConceptsAtrial arteriolesBlood cardioplegiaVasomotor regulationSubstance PCOX-2Constitutive endothelial nitric oxide synthaseNitric oxideEndothelial nitric oxide synthaseCoronary microvascular regulationHyperkalemic blood cardioplegiaPotent contractile responseEndothelium-independent relaxationCoronary artery surgeryCoronary bypass surgeryEndothelium-dependent relaxationCoronary artery diseaseNitric oxide synthaseReverse transcriptase-polymerase chain reactionRelease of prostaglandinsBrief reperfusionCoronary contractionArtery surgeryCoronary spasmBypass surgeryContractile responseLocal Perivascular Delivery of Basic Fibroblast Growth Factor in Patients Undergoing Coronary Bypass Surgery
Laham R, Sellke F, Edelman E, Pearlman J, Ware J, Brown D, Gold J, Simons M. Local Perivascular Delivery of Basic Fibroblast Growth Factor in Patients Undergoing Coronary Bypass Surgery. Circulation 1999, 100: 1865-1871. PMID: 10545430, DOI: 10.1161/01.cir.100.18.1865.Peer-Reviewed Original ResearchMeSH KeywordsAlginatesCoronary Artery BypassCoronary VesselsDelayed-Action PreparationsDouble-Blind MethodDrug CarriersDrug CompoundingDrug ImplantsFemaleFibroblast Growth Factor 2Follow-Up StudiesGlucuronic AcidHeparinHexuronic AcidsHumansMaleMiddle AgedPatient SelectionPlacebosRecombinant ProteinsConceptsBasic fibroblast growth factorBFGF groupFibroblast growth factorTreatment-related adverse eventsQ-wave myocardial infarctionGrowth factorLocal perivascular deliverySerum bFGF levelsPlacebo-controlled studyCoronary bypass surgerySubset of patientsMode of therapyMagnetic resonance assessmentPromising treatment strategyNuclear perfusionOperative deathsRecurrent anginaStandard revascularizationNew blood vesselsPlacebo groupRepeat revascularizationAdverse eventsBypass surgeryControl patientsPerivascular deliveryAttenuation of Endothelium-Dependent Dilation of Pig Pulmonary Arterioles After Cardiopulmonary Bypass Is Prevented by Monoclonal Antibody to Complement C5a
Park K, Tofukuji M, Metais C, Comunale M, Dai H, Simons M, Stahl G, Agah A, Sellke F. Attenuation of Endothelium-Dependent Dilation of Pig Pulmonary Arterioles After Cardiopulmonary Bypass Is Prevented by Monoclonal Antibody to Complement C5a. Anesthesia & Analgesia 1999, 89: 42-48.. DOI: 10.1213/00000539-199907000-00008.Peer-Reviewed Original ResearchConceptsNitric oxide synthasePulmonary endothelial dysfunctionCardiopulmonary bypassEndothelial dysfunctionMonoclonal antibodiesPulmonary arteriolesComplement C5aPrevious administrationConstitutive nitric oxide synthaseAnti-C5a monoclonal antibodyEndothelium-dependent dilatorsEndothelium-dependent dilationTissue myeloperoxidase activityNormothermic cardiopulmonary bypassReverse transcriptase-polymerase chain reactionTranscriptase-polymerase chain reactionNeutrophil sequestrationMyeloperoxidase activityMPO activityPolymerase chain reactionSubstance POxide synthaseSodium nitroprussideComplement activationRelaxation responseAttenuation of endothelium-dependent dilation of pig pulmonary arterioles after cardiopulmonary bypass is prevented by monoclonal antibody to complement C5a.
Park K, Tofukuji M, Metais C, Comunale M, Dai H, Simons M, Stahl G, Agah A, Sellke F. Attenuation of endothelium-dependent dilation of pig pulmonary arterioles after cardiopulmonary bypass is prevented by monoclonal antibody to complement C5a. Anesthesia & Analgesia 1999, 89: 42-8. PMID: 10389776, DOI: 10.1097/00000539-199907000-00008.Peer-Reviewed Original ResearchSubxyphoid access of the normal pericardium: A novel drug delivery technique
Laham R, Simons M, Hung D. Subxyphoid access of the normal pericardium: A novel drug delivery technique. Catheterization And Cardiovascular Interventions 1999, 47: 109-111. PMID: 10385173, DOI: 10.1002/(sici)1522-726x(199905)47:1<109::aid-ccd24>3.0.co;2-3.Peer-Reviewed Original ResearchConceptsPericardial spaceHemodynamic compromiseNormal pericardiumSubxyphoid accessSmall pericardial effusionContinuous positive pressureNovel drug delivery techniqueIntrapericardial drug deliveryAnimals 4 weeksLarge animal modelDelivery techniquesNovel delivery techniquesAdverse eventsPericardial effusionMyocardial damageDrug delivery techniquesRight ventricleFluoroscopic guidanceInfusion catheterHistologic examinationPericardial accessIntroducer needlePositive pressureHigh riskAnimal modelsEffect of sialyl Lewisx oligosaccharide on myocardial and cerebral injury in the pig
Tofukuji M, Metais C, Collard C, Morse D, Stahl G, Nelson D, Li J, Simons M, Sellke F. Effect of sialyl Lewisx oligosaccharide on myocardial and cerebral injury in the pig. The Annals Of Thoracic Surgery 1999, 67: 112-119. PMID: 10086534, DOI: 10.1016/s0003-4975(98)01130-8.Peer-Reviewed Original ResearchConceptsArtery blood flowCardiopulmonary bypassMyeloperoxidase activityBrain arteriolesNeutrophil infiltrationOrgan perfusionBlood flowInducible isoformInternal carotid artery blood flowEndothelium-dependent relaxation responsesCoronary artery blood flowCarotid artery blood flowLeft ventricular systolic pressureNitric oxide synthase mRNAAdministration of CYBeneficial acute effectsCerebral vascular resistanceEndothelium-independent relaxationEndothelium-dependent relaxationVentricular systolic pressureCoronary artery occlusionMyocardial contractile functionNormothermic cardiopulmonary bypassLeft ventricular pressureNitric oxide synthase
1998
Anti-C5a monoclonal antibody reduces cardiopulmonary bypass and cardioplegia-induced coronary endothelial dysfunction
Tofukuji M, Stahl G, Agah A, Metais C, Simons M, Sellke F, This study was supported by National Institutes of Health grants HL46716 H. Anti-C5a monoclonal antibody reduces cardiopulmonary bypass and cardioplegia-induced coronary endothelial dysfunction. Journal Of Thoracic And Cardiovascular Surgery 1998, 116: 1060-1068. PMID: 9832699, DOI: 10.1016/s0022-5223(98)70059-5.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, MonoclonalCardiopulmonary BypassChemotaxis, LeukocyteComplement C5aCoronary VesselsEndothelium, VascularFemaleHeart Arrest, InducedHemodynamicsMaleMiceMice, Inbred BALB CMyocardial Reperfusion InjuryNeutrophilsNitric Oxide SynthaseNitric Oxide Synthase Type IINitric Oxide Synthase Type IIIPeroxidaseSwineConceptsEndothelium-dependent relaxationSaline solution groupCardiopulmonary bypassMonoclonal antibodiesCardioplegic reperfusionSolution groupImpaired endothelium-dependent relaxationAnti-C5a monoclonal antibodyCoronary endothelial dysfunctionPolymorphonuclear leukocyte infiltrationLeft ventricular pressureSaline solution vehiclePercent segmental shorteningMonoclonal antibody groupC5a inhibitionEndothelial dysfunctionMyeloperoxidase activityCoronary arteriolesLeukocyte infiltrationSegmental shorteningCoronary arteryHyperkalemic cardioplegiaFunctional preservationVentricular pressureVascular studies