2004
Cardiac myocyte‐specific HIF‐1α deletion alters vascularization, energy availability, calcium flux, and contractility in the normoxic heart
Huang Y, Hickey RP, Yeh JL, Liu D, Dadak A, Young LH, Johnson RS, Giordano FJ. Cardiac myocyte‐specific HIF‐1α deletion alters vascularization, energy availability, calcium flux, and contractility in the normoxic heart. The FASEB Journal 2004, 18: 1138-1140. PMID: 15132980, DOI: 10.1096/fj.04-1510fje.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCalcium SignalingCoronary CirculationDNA-Binding ProteinsEnergy MetabolismGene DeletionGene Expression RegulationHeart Function TestsHypoxia-Inducible Factor 1Hypoxia-Inducible Factor 1, alpha SubunitMiceMice, Inbred C57BLMice, KnockoutMyocardial ContractionMyocardiumMyocytes, CardiacNeovascularization, PhysiologicNuclear ProteinsOxygen ConsumptionReverse Transcriptase Polymerase Chain ReactionRNA, MessengerTranscription FactorsTranscription, GeneticConceptsCardiac functionCalcium fluxHypoxia-inducible transcription factor HIF-1alphaCardiac oxygen deliveryDisease statesHIF-1alphaSkeletal muscleCardiac contractile dysfunctionHigh-energy phosphate contentCardiovascular disease statesResting pulse rateTranscription factor HIF-1alphaCoronary vasodilatationMyocardial demandContractile dysfunctionMyocardial hibernationNormoxic heartsOxygen supplyGene expressionCalcium handlingOxygen deliveryPulse rateHeart muscleCardiac muscleMolecular pathology
1995
Technetium-99m-nitroimidazole (BMS181321): a positive imaging agent for detecting myocardial ischemia.
Shi CQ, Sinusas AJ, Dione DP, Singer MJ, Young LH, Heller EN, Rinker BD, Wackers FJ, Zaret BL. Technetium-99m-nitroimidazole (BMS181321): a positive imaging agent for detecting myocardial ischemia. Journal Of Nuclear Medicine 1995, 36: 1078-86. PMID: 7769431.Peer-Reviewed Original ResearchConceptsIschemic regionMyocardial ischemiaBlood flowEx vivo SPECTRegional myocardial blood flowPartial coronary occlusionMicrosphere blood flowMyocardial blood flowOpen-chest canine modelVivo SPECT imagesSPECT imagesVivo planarCentral ischemic regionCoronary occlusionDemand ischemiaBMS181321Technetium-99mIntravenous injectionLiver ratioMyocardial imagingCanine modelPositive imagingHepatic clearanceLiver activityArterial sampling
1991
Myocardial protein turnover in patients with coronary artery disease. Effect of branched chain amino acid infusion.
Young LH, McNulty PH, Morgan C, Deckelbaum LI, Zaret BL, Barrett EJ. Myocardial protein turnover in patients with coronary artery disease. Effect of branched chain amino acid infusion. Journal Of Clinical Investigation 1991, 87: 554-560. PMID: 1991838, PMCID: PMC296343, DOI: 10.1172/jci115030.Peer-Reviewed Original ResearchMeSH KeywordsAgedAmino Acids, Branched-ChainCoronary DiseaseFemaleGlucoseHeartHumansLactatesLactic AcidMaleMiddle AgedMyocardiumOxygen ConsumptionProteinsConceptsBranched-chain amino acid infusionCoronary artery diseaseAmino acid infusionProtein turnoverBCAA infusionProtein synthesisArtery diseaseAcid infusionAmino acidsMyocardial protein turnoverCardiac double productCoronary blood flowPlasma insulin levelsMyocardial oxygen consumptionHuman heartProtein degradationNegative protein balanceEssential amino acidsMyocardial balanceInsulin levelsDouble productPhenylalanine balanceAnabolic effectsMyocardial uptakePostabsorptive patients