Alpha and beta adrenergic interactions with ouabain-induced delayed afterdepolarizations

Area of Science:

• Cardiovascular Physiology
• Cardiac Electrophysiology
• Pharmacology

Background:

• Ouabain toxicity can induce dangerous cardiac arrhythmias.
• Delayed afterdepolarizations (DADs) are implicated in arrhythmogenesis.
• Adrenergic signaling plays a role in cardiac function and arrhythmogenesis.

Purpose of the Study:

• To investigate the role of alpha and beta-adrenergic signaling in ouabain-induced DADs.
• To determine the effects of adrenergic agonists and antagonists on canine Purkinje fiber DADs.

Main Methods:

• Standard microelectrode techniques were employed.
• Isolated canine Purkinje fibers were superfused with ouabain to induce DADs.
• Fibers were subsequently exposed to alpha and beta-adrenergic agonists and antagonists.

Main Results:

• Beta-adrenergic stimulation (isoproterenol) increased DAD amplitude and triggered activity.
• Higher concentrations of propranolol (beta-blocker) reduced DADs and eliminated triggered rhythms.
• Alpha-adrenergic blockade (phentolamine) and agonist (methoxamine) had no significant effect.

Conclusions:

• Beta-adrenergic stimulation can exacerbate DADs and triggered activity in ouabain-toxic Purkinje fibers.
• Alpha-adrenergic agents do not appear to significantly influence ouabain-induced DADs or triggered rhythms.