2003
Nitrotyrosine and 8-isoprostane formation indicate free radical-mediated injury in hearts of patients subjected to cardioplegia
Mehlhorn U, Krahwinkel A, Geissler H, LaRosee K, Fischer U, Klass O, Suedkamp M, Hekmat K, Tossios P, Bloch W. Nitrotyrosine and 8-isoprostane formation indicate free radical-mediated injury in hearts of patients subjected to cardioplegia. Journal Of Thoracic And Cardiovascular Surgery 2003, 125: 178-183. PMID: 12539002, DOI: 10.1067/mtc.2003.97.Peer-Reviewed Original ResearchConceptsEnd of bypassCardiopulmonary bypassCyclic guanosine monophosphateMyocardial ischemiaIntermittent cold blood cardioplegiaConstitutive nitric oxide synthaseNitric oxide synthase activityNitric oxide synthase activationCyclic guanosine monophosphate contentOxygen-derived free radicalsCardiac myocytesCoronary endothelial injuryCoronary artery operationsFree radical-mediated lipid peroxidationCold blood cardioplegiaFree radical-mediated injuryGuanosine monophosphateHearts of patientsOxide synthase activityNitric oxide synthaseRadical-mediated lipid peroxidationVentricular biopsy specimensRadical-mediated injuryNitric oxide releaseBlood cardioplegia
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 response
1998
Effects 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
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