2001
Serotonin-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
Molecular multitasking: statins lead to more arteries, less plaque
Simons M. Molecular multitasking: statins lead to more arteries, less plaque. Nature Medicine 2000, 6: 965-966. PMID: 10973306, DOI: 10.1038/79646.Peer-Reviewed Original ResearchAnticholesteremic AgentsArteriosclerosisEnzyme ActivationHydroxymethylglutaryl-CoA Reductase InhibitorsNeovascularization, PhysiologicNitric Oxide SynthaseNitric Oxide Synthase Type IIIProtein KinasesProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktSignal TransductionSimvastatinBasic 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
Attenuation 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 Research
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 studiesEffects of coronary artery disease on expression and microvascular response to VEGF
Métais C, Li J, Li J, Simons M, Sellke F. Effects of coronary artery disease on expression and microvascular response to VEGF. American Journal Of Physiology 1998, 275: h1411-h1418. PMID: 9746492, DOI: 10.1152/ajpheart.1998.275.4.h1411.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine DiphosphateCell DivisionCoronary Artery BypassCoronary DiseaseEndothelial Growth FactorsEndothelium, VascularFemaleGene Expression RegulationGenisteinHeart AtriaHepatocyte Growth FactorHumansIn Vitro TechniquesKineticsLymphokinesMaleMicrocirculationMicroscopy, VideoMiddle AgedMuscle RelaxationMuscle, Smooth, VascularNitric Oxide SynthaseNitric Oxide Synthase Type IINitric Oxide Synthase Type IIINitroarginineProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesReceptors, Growth FactorReceptors, MitogenReceptors, Vascular Endothelial Growth FactorRNA, MessengerTranscription, GeneticVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1Vascular Endothelial Growth FactorsVasodilationConceptsCoronary artery diseaseInducible nitric oxide synthaseConstitutive nitric oxide synthaseVascular endothelial growth factorHepatocyte growth factorExpression of VEGFNitric oxide synthaseArtery diseaseNG-nitroMicrovascular responsesOxide synthaseExpression of cNOSL-arginineGrowth factorCoronary microvascular responsesSubstance P responseExogenous vascular endothelial growth factorEndothelial growth factorFlk-1 receptorFlt-1 receptorMild hypercholesterolemiaTyrosine kinase receptorsTyrosine kinase inhibitor genisteinEndothelium dysfunctionVascular responses