Ventricular Dysfunction After Cardioplegic Arrest Is Improved After Myocardial Gene Transfer of a β-Adrenergic Receptor Kinase Inhibitor | Zendy

Hendrik T. Tevaearai | Zendy; Andrea D. Eckhart | Zendy; Kyle F. Shotwell | Zendy; Katrina H. Wilson | Zendy; Walter J. Koch | Zendy

Open Access

Ventricular Dysfunction After Cardioplegic Arrest Is Improved After Myocardial Gene Transfer of a β-Adrenergic Receptor Kinase Inhibitor

Author(s) -

Hendrik T. Tevaearai,

Andrea D. Eckhart,

Kyle F. Shotwell,

Katrina H. Wilson,

Walter J. Koch

Publication year - 2001

Publication title -

circulation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 7.795

H-Index - 607

eISSN - 1524-4539

pISSN - 0009-7322

DOI - 10.1161/hc4201.097188

Subject(s) - medicine , preload , contractility , cardiology , cardiopulmonary bypass , cardiac function curve , ventricular assist device , adrenergic , anesthesia , heart failure , receptor , hemodynamics

Acute cardiac contractile dysfunction is common after cardiopulmonary bypass (CPB). A potential molecular mechanism is enhanced beta-adrenergic receptor kinase (betaARK1) activity, because beta-adrenergic receptor (betaAR) signaling is altered in cardiomyocytes after cardioplegia. Therefore, we examined whether adenovirus-mediated intracoronary delivery of a betaARK1 inhibitor (Adv-betaARKct) could prevent post-CPB dysfunction.

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