Abstract
The present study examined the ventricular arrhythmic and electrophysiological properties during hyperkalemia (6.3 mM [K+] vs. 4 mM in normokalemia) and anti-arrhythmic effects of hypercalcemia (2.2 mM [Ca2+]) in Langendorff-perfused mouse hearts. Monophasic action potential recordings were obtained from the left ventricle during right ventricular pacing. Hyperkalemia increased the proportion of hearts showing provoked ventricular tachycardia (VT) from 0 to 6 of 7 hearts during programmed electrical stimulation (Fisher's exact test, P<0.05). It shortened the epicardial action potential durations (APDx) at 90, 70, 50 and 30% repolarization and ventricular effective refractory periods (VERPs) (analysis of variance, P<0.05) without altering activation latencies. Endocardial APDx and VERPs were unaltered. Consequently, ∆APDx (endocardial APDx-epicardial APDx) was increased, VERP/latency ratio was decreased and critical intervals for reexcitation (APD90-VERP) were unchanged. Hypercalcemia treatment exerted anti-arrhythmic effects during hyperkalemia, reducing the proportion of hearts showing VT to 1 of 7 hearts. It increased epicardial VERPs without further altering the remaining parameters, returning VERP/latency ratio to normokalemic values and also decreased the critical intervals. In conclusion, hyperkalemia exerted pro-arrhythmic effects by shortening APDs and VERPs. Hypercalcemia exerted anti-arrhythmic effects by reversing VERP changes, which scaled the VERP/latency ratio and critical intervals.
Highlights
The extracellular potassium concentration ([K+]o) is normally maintained between 3.5 and 5 mM
Ventricular arrhythmogenicity and its associations to action potential characteristics were examined under normokalemia (5.2 mM [K+]), normocalcemia (1.8 mM [Ca2+]), hyperkalemia alone (6.3 mM [K+]) and hyperkalemia with hypercalcemia treatment (2.2 mM [Ca2+])
The initial experiments were performed on hearts extrinsically paced at 8 Hz, which is close to the heart rate observed in vivo under normokalemic, hyperkalemic and combined hyperkalemic and hypercalcemic conditions
Summary
The extracellular potassium concentration ([K+]o) is normally maintained between 3.5 and 5 mM. There have been certain previous studies on the electrophysiological changes during hyperkalemia [13,14], but not on the mechanism underlying the anti‐arrhythmic action of calcium in this situation, apart from its ‘membrane‐stabilizing effect’ [15]. This notion has been disputed and the protective action of high [Ca2+]o has instead been attributed to restoration of conduction velocities (CVs) back to normal values [16]
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