Beta Receptor Blockade Potentiates the Antiarrhythmic Actions of d‐Sotalol on Reentrant Ventricular Tachycardia in a Canine Model of Myocardial Infarction

@article{Kassotis2003BetaRB,
  title={Beta Receptor Blockade Potentiates the Antiarrhythmic Actions of d‐Sotalol on Reentrant Ventricular Tachycardia in a Canine Model of Myocardial Infarction},
  author={John Kassotis and Roy Sauberman and Candido Cabo and Andrew L. Wit and James Coromilas},
  journal={Journal of Cardiovascular Electrophysiology},
  year={2003},
  volume={14}
}
Introduction: The importance of beta receptor blockade for the antiarrhythmic action of sotalol has not been completely elucidated. We determined how beta receptor blockade interacts with the effects of potassium channel blockade on reentrant circuits. 
Electrophysiologic Actions of d,l-Sotalol and GLG-V-13 in Ischemically Injured Canine Epicardium
TLDR
A variable response of ischemically injured canine epicardial cells to action potential prolongation with GLG-V-13 and d,l-sotalol is demonstrated, facilitating localized reentry in vitro, despite a failure of the same drugs to facilitate reentrant tachycardia in vivo.
Regadenoson, a Novel Pharmacologic Stress Agent for Use in Myocardial Perfusion Imaging, Does Not Have a Direct Effect on the QT Interval in Conscious Dogs
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Regadenoson at 5 and 10 μg/kg did not cause a significant change in HR or QT interval either during atrial pacing at 165 bpm or after administration of propranolol and atropine to prevent HR from changing or after treatment of dogs with hexamethonium to block autonomic ganglia.
POSITIVE RATE DEPENDENT ACTION POTENTIAL PROLONGATION BY MODULATING POTASSIUM ION CHANNELS
  • C. Cabo
  • Biology, Medicine
    bioRxiv
  • 2022
TLDR
In computer models of the ventricular action potential, the use of a combination of IKs activators and IKr and Ik1 blockers could result in APD prolongation that potentially maximizes anti-arrhythmic effects and minimizes pro-arrhinic effects.
Myeloid Cell Sirtuin-1 Expression Does Not Alter Host Immune Responses to Gram-Negative Endotoxemia or Gram-Positive Bacterial Infection
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It is demonstrated that myeloid SIRT1 expression does not change mortality in gram-negative toxin-induced shock or gram-positive bacteremia, suggesting that therapeutic suppression of Sirtuin-1 may be done safely without suppression of myeloids cell-specific immune responses to severe bacterial infections.

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