Mechanism of Calcium Induced Fibrillation in the Toad's Heart

Mechanisms of occurrence of the fibrillation induced in the toad's heart by excess calcium in Ringer's solution were studied by measuring the threshold current, the conduction velocity, the absolute refractory period and the transmembrane potential.2. In the ventricle, excess calcium in Ringer's solution elevated the threshold current, slowed the conduction velocity and shortened the absolute refractory period. When the height of the action potential was reduced, the maximum rate of depolarization decreased and the duration of the action potential shortened without altering the level of the resting potential. At about 7 times the normal [Ca]o, fibrillation occurred in response to a single stimulus.3. Sodium or potassium deficiency in Ringer's solution potentiated the cardiac effect of excess calcium and facilitated the occurrence of fibrillation. On the contrary, excess potassium in the perfusing fluid antagonized it.4. These results were interpreted as indicating that:(a) Effects of excess calcium on the cardiac excitability are caused by the suppression of sodium permeability of the membrane during excitation, and (b) The mechanism of fibrillation might be due to a reentry of excitation.5. The atrium required much higher [Ca]o (about 10 times the normal value) for an induction of fibrillation. Application of acetylcholine or potassium deficiency in Ringer's solution facilitated an induction of fibrillation. Difficulty to induce fibrillation in the atrium only by excess calcium indicates the relatively lower sensitivity to excess calcium than in the ventricle. In addition, slight prolongation of the absolute refractory period by excess calcium was observed in the atrium. The fact that the atrial tissue contains more calcium but less potassium than the ventricular ones suggests the different sensitivity to excess calcium between them.