High-calcium exposure to frog heart: a simple model representing hypercalcemia-induced ECG abnormalities

Figures

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  Fig. 1.. Simultaneous recordings of the transmembrane action potential and electrocardiogram (ECG) in the bullfrog heart. The top trace shows the action potential of ventricular cardiomyocytes, which consists of phases including “overshoot” (phase 0), “slow repolarization” (combined phase 1 and 2: partial repolarization immediately followed by the plateau phase), “rapid repolarization” (phase 3) and “resting membrane potential” (phase 4). The bottom trace illustrates the ECG with P waves followed by prominent QRS complexes and biphasic T waves.

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  Fig. 2.. Effects of high-calcium exposure to the bullfrog heart. CaCl2 solution (1 M) was added externally to immerse the exposed ventricular surface of the frog heart. Shortly (2 min) (A) and long (30 min) (B) after such high-calcium exposure, the action potential of ventricular cardiomyocytes (top) and the ECG waves (bottom) were simultaneously recorded.

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  Fig. 3.. Mechanisms by which high-calcium exposure decreases the duration of the total systolic phase of the action potential. Action potentials 2 min (dashed line) and 30 min (dotted line) after 1 M CaCl2 was added externally onto the ventricular surface of frog hearts. Generally, the duration of phase 3 (rapid repolarization) of the action potential is determined by the outward potassium flow through the “delayed rectifier potassium channels”. However, the rise in extracellular calcium concentration, which facilitates the intracellular entry of calcium ions, stimulates “calcium-activated potassium channels,” such as large conductance and small conductance K+ channels. This would increase the outward potassium currents during phase 3 of the action potential, accelerating the process of repolarization and thus decreasing the total duration of the systolic phase.