Postcountershock fibrillation in digitalized myocardial cells in vitro

Area of Science:

• Cardiology
• Electrophysiology
• Cell Biology

Background:

• Digitalis use potentiates postcountershock arrhythmias, often leading to fatal ventricular fibrillation.
• The underlying mechanisms for this potentiation remain largely unknown.
• Previous hypotheses suggested secondary mechanisms, such as nervous system effects.

Purpose of the Study:

• To investigate if ouabain (a digitalis glycoside) accentuates electric shock-induced arrhythmias in isolated myocardial cells.
• To determine if potentiation occurs at the cellular level, rather than via systemic effects.

Main Methods:

• Cultured in vitro myocardial cells were subjected to electric field stimulation.
• Ouabain was administered at varying concentrations, from therapeutic to toxic levels.
• Postshock arrhythmias and cellular fibrillation were assessed using a photovoltaic cell and video monitoring.

Main Results:

• Low concentrations of ouabain (5 x 10(-8)M to 7 x 10(-6)M) increased the duration of postshock arrest.
• Cellular fibrillation was induced by low-intensity electric shocks in cells exposed to low ouabain concentrations, a phenomenon not observed when either stimulus was applied alone.
• These findings parallel previously observed cellular fibrillation after high shocks or toxic ouabain levels.

Conclusions:

• The deleterious interaction between digitalis and electric countershock occurs directly within the myocardial cell.
• Postshock cellular fibrillation in vitro may underlie the "unmasking" of digitalis toxicity observed clinically.
• This cellular mechanism provides insight into the potentiation of arrhythmias and fatal outcomes.