D
David A. Kass
Researcher at Johns Hopkins University School of Medicine
Publications - 605
Citations - 63963
David A. Kass is an academic researcher from Johns Hopkins University School of Medicine. The author has contributed to research in topics: Heart failure & Cardiac resynchronization therapy. The author has an hindex of 127, co-authored 580 publications receiving 58747 citations. Previous affiliations of David A. Kass include University of Pittsburgh & Johns Hopkins University.
Papers
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Journal ArticleDOI
Determinants of shear stress-stimulated endothelial nitric oxide production assessed in real-time by 4,5-diaminofluorescein fluorescence.
TL;DR: It is revealed that DAF-2 can assess real-time SS-stimulated NO synthesis in endothelial cells and facilitate the analysis of NO-signaling pathways, providing novel insights into several NO signaling determinants.
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TRP-ing up heart and vessels: canonical transient receptor potential channels and cardiovascular disease.
TL;DR: New evidence supporting a pathophysiologic role of these three TRPC channels is described, and the potential utility of inhibition strategies to treat cardiovascular disease is described.
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Cardiac nitric oxide production due to angiotensin-converting enzyme inhibition decreases beta-adrenergic myocardial contractility in patients with dilated cardiomyopathy
Ilan S. Wittstein,David A. Kass,Peter H. Pak,W. Lowell Maughan,Barry J. Fetics,Joshua M. Hare +5 more
TL;DR: Enalaprilat attenuates beta-adrenergic contractility and enhances left ventricular distensibility in patients with idiopathic dilated cardiomyopathy, but not in subjects with normalleft ventricular function.
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Pressure-volume analysis of changes in cardiac function in chronic cardiomyoplasty
Peter W. Cho,Howard R. Levin,William E. Curtis,Joshua E. Tsitlik,DiNatale Jm,David A. Kass,Timothy J. Gardner,Ralph W. Kunel,Michael A. Acker +8 more
TL;DR: Assessment of the primary functional properties of the heart wrapped by conditioned muscle using pressure-volume relation analysis based on conductance catheter volume data concludes that in the nonfailing heart, increased contractility does not augment cardiac output, ejection fraction, and stroke work because of a simultaneous decrease in end-diastolic volume.
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Peroxynitrite and myocardial contractility: in vivo versus in vitro effects.
Tatsuo Katori,Sonia Donzelli,Carlo G. Tocchetti,Katrina M. Miranda,Gianfrancesco Emanuele Cormaci,Douglas D. Thomas,Elizabeth A. Ketner,Myung Jae Lee,Daniele Mancardi,David A. Wink,David A. Kass,Nazareno Paolocci +11 more
TL;DR: Systemic generation of ONOO- is unlikely to have primary cardiac effects, but may modulate cardiac contractile reserve, via blunted beta-adrenergic stimulation, and vascular tone, as a result of generation of NO2- and NO3-.