Downstream defects in beta-adrenergic signaling and relation to myocyte contractility after cardioplegic arrest

The Journal of Thoracic and Cardiovascular Surgery
W V HouckF G Spinale

Abstract

Transient left ventricular dysfunction can occur after hypothermic, hyperkalemic cardioplegic arrest and is associated with decreased beta-adrenergic receptor responsiveness. Occupancy of the beta-adrenergic receptor activates adenylate cyclase, which phosphorylates the L-type Ca2+ channel-enhancing myocyte contractility. The goal of this study was to identify potential mechanisms that contribute to the defects in the beta-adrenergic receptor signaling cascade after cardioplegic arrest. Isolated left ventricular porcine myocytes were assigned to one of two treatment groups: (1) cardioplegic arrest (24 mEq/L K+, 4 degrees C x 2 hours, then 5 minutes in 37 degrees C cell media; n = 130) or (2) normothermic control (cell media, 37 degrees C x 2 hours; n = 222). Myocyte contractility was assessed at baseline and after either beta-adrenergic receptor occupancy (25 nmol/L isoproterenol [INN: isoprenaline]), activation of adenylate cyclase (0.5 mumol forskolin), or direct activation of the L-type Ca(2+)-channel (10 nmol/L or 100 nmol/L (-)BayK 8644). Myocyte velocity of shortening (micron/sec) was increased with beta-adrenergic receptor occupancy or direct adenylate cyclase stimulation compared with baseline in the normothermic group ...Continue Reading

References

Oct 8, 1992·The American Journal of Cardiology·A M Katz
Jan 1, 1988·Progress in Biophysics and Molecular Biology·H C Hartzell
Jul 22, 1982·The New England Journal of Medicine·M R BristowE B Stinson
Jul 1, 1984·The Journal of Clinical Investigation·M R BristowW Minobe
Sep 1, 1996·The Journal of Thoracic and Cardiovascular Surgery·J R LópezA Terzic

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