Acetylcholine-calcium interactions in the canine atrium and sinus node.
Although the enhancement of acetylcholine release by extracellular calcium is well recognized, the potential arrhythmogenicity of vagal-calcium interactions has not been studied. We used anesthetized mongrel dogs and recorded: ECG, arterial pressure, and electrograms from the sinus node, sulcus terminalis, right atrium, right ventricle, and His bundle. All animals were autonomically decentralized. The sinus node artery was catheterized, its distribution was verified, and it was autologously perfused via the femoral artery. Vagal stimulation was carried out during autologous blood perfusion of the sinus node artery and again during perfusion with oxygenated Tyrode solution, with calcium concentrations ranging from 1.8 to 16.2 mmol. Vagal slowing of rate was accentuated in the presence of calcium concentrations as low as 2.7 mmol. Further increments in calcium concentration resulted in vagally-induced atrial fibrillation. Fibrillation was characterized by rapid, regular repetitive activity which was superceded by chaotic atrial rhythm at about 10 seconds and blocked by atropine. Elevations in calcium alone (5.4 to 16.2 mmol) resulted in atrial fibrillation which was chaotic in appearance and not blocked by atropine. We conclude that increases in calcium concentration within the distribution of the sinus node artery are arrhythmogenic alone, and also enhance vagally-induced changes in atrial rhythmicity.
D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D001281:Atrial Fibrillation / Q000139:chemically induced / Q000503:physiopathology; D001285:Atropine / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism / Q000502:physiology*; D004285:Dogs; D004347:Drug Interactions; D004562:Electrocardiography; D012849:Sinoatrial Node / Q000187:drug effects / Q000503:physiopathology*; D014630:Vagus Nerve / Q000187:drug effects
D001285:Atropine; D000109:Acetylcholine; D002118:Calcium