Acetylcholine-calcium interactions in the canine atrium and sinus node.

Area of Science:

• Cardiology
• Electrophysiology
• Pharmacology

Background:

• Extracellular calcium enhances acetylcholine release, a key neurotransmitter in cardiac regulation.
• The arrhythmogenic potential of vagal-calcium interactions in the heart remains largely uninvestigated.

Purpose of the Study:

• To investigate the arrhythmogenic effects of varying calcium concentrations on vagal stimulation in the canine heart.
• To determine if elevated calcium levels alone can induce cardiac arrhythmias.

Main Methods:

• Anesthetized mongrel dogs with decentralized autonomic nervous systems were used.
• Electrophysiological recordings (ECG, arterial pressure, various electrograms) were obtained.
• The sinus node artery was perfused with solutions containing varying calcium concentrations (1.8–16.2 mmol) during vagal stimulation.

Main Results:

• Vagal stimulation at lower calcium concentrations (2.7 mmol) accentuated heart rate slowing.
• Higher calcium concentrations induced vagally-mediated atrial fibrillation, initially regular then chaotic, blocked by atropine.
• Elevated calcium levels (5.4–16.2 mmol) alone caused chaotic atrial fibrillation, unresponsive to atropine.

Conclusions:

• Increased sinus node artery calcium concentration is arrhythmogenic independently.
• Calcium enhances vagally-induced alterations in atrial rhythmicity, contributing to arrhythmia development.