Reduction in vulnerability to ventricular fibrillation by bromocriptine, a dopamine agonist

Area of Science:

• Cardiology
• Pharmacology
• Neuroscience

Background:

• Ventricular fibrillation (VF) is a life-threatening arrhythmia.
• Dopamine agonists and antagonists are known to affect cardiovascular function.
• The specific role of dopamine in modulating cardiac electrical stability, particularly VF threshold, requires further elucidation.

Purpose of the Study:

• To investigate the effect of the dopamine agonist bromocriptine on the ventricular fibrillation threshold in a canine model.
• To determine if dopamine receptor blockade can abolish the effects of bromocriptine on VF threshold.

Main Methods:

• Anesthetized dogs were used as the experimental model.
• Ventricular fibrillation threshold (VFT) was measured.
• The effects of bromocriptine administration on VFT were assessed.
• The influence of pretreatment with dopamine antagonists (haloperidol and domperidone) on bromocriptine's effects was evaluated.

Main Results:

• Bromocriptine administration resulted in a 50% increase in the ventricular fibrillation threshold.
• Pretreatment with haloperidol, a central and peripheral dopamine antagonist, abolished the increase in VFT caused by bromocriptine.
• Pretreatment with domperidone, a peripheral dopamine antagonist, also abolished the effects of bromocriptine on VFT.

Conclusions:

• Bromocriptine reduces the vulnerability of the non-ischemic canine ventricle to fibrillation.
• The anti-fibrillatory effect of bromocriptine appears to be mediated by peripheral dopaminergic receptors.
• This effect is likely due to the inhibition of noradrenaline release via presynaptic dopaminergic stimulation.