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Anti-arrhythmic effects of hypercalcemia in hyperkalemic, Langendorff-perfused mouse hearts

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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.

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Representative epicardial MAP recordings from programmed electrical stimulation (PES) under (A) control conditions, and (B) hyperkalemia alone and (C) following hypercalcemia treatment. (D) The incidences of provoked ventricular tachycardia (VT) demonstrate the pro-arrhythmic effects of hyperkalemia (Fisher's exact test, **P<0.01) and the subsequent anti-arrhythmic effects of hypercalcemia treatment (Fisher's exact test, ††P<0.01). MAP, monophasic action potential.
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f2-br-0-0-735: Representative epicardial MAP recordings from programmed electrical stimulation (PES) under (A) control conditions, and (B) hyperkalemia alone and (C) following hypercalcemia treatment. (D) The incidences of provoked ventricular tachycardia (VT) demonstrate the pro-arrhythmic effects of hyperkalemia (Fisher's exact test, **P<0.01) and the subsequent anti-arrhythmic effects of hypercalcemia treatment (Fisher's exact test, ††P<0.01). MAP, monophasic action potential.

Mentions: PES delivering progressively premature stimuli was used to examine the arrhythmic tendency. It consistently failed to provoke any arrhythmia under the control conditions (Fig. 2A; S2 extrastimulus indicated by an arrow). By contrast, provoked ventricular tachycardia (VT) was observed under hyperkalemic conditions alone (Fig. 2B). This was prevented by further hypercalcemia treatment (Fig. 2C). The incidences of provoked VT observed are summarized in Fig. 2D, demonstrating that hyperkalemia was significantly arrhythmogenic (Fisher's exact test, P<0.01), whereas hypercalcemia treatment was anti-arrhythmic under hyperkalemic conditions (Fisher's exact test, P<0.01).


Anti-arrhythmic effects of hypercalcemia in hyperkalemic, Langendorff-perfused mouse hearts
Representative epicardial MAP recordings from programmed electrical stimulation (PES) under (A) control conditions, and (B) hyperkalemia alone and (C) following hypercalcemia treatment. (D) The incidences of provoked ventricular tachycardia (VT) demonstrate the pro-arrhythmic effects of hyperkalemia (Fisher's exact test, **P<0.01) and the subsequent anti-arrhythmic effects of hypercalcemia treatment (Fisher's exact test, ††P<0.01). MAP, monophasic action potential.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4998139&req=5

f2-br-0-0-735: Representative epicardial MAP recordings from programmed electrical stimulation (PES) under (A) control conditions, and (B) hyperkalemia alone and (C) following hypercalcemia treatment. (D) The incidences of provoked ventricular tachycardia (VT) demonstrate the pro-arrhythmic effects of hyperkalemia (Fisher's exact test, **P<0.01) and the subsequent anti-arrhythmic effects of hypercalcemia treatment (Fisher's exact test, ††P<0.01). MAP, monophasic action potential.
Mentions: PES delivering progressively premature stimuli was used to examine the arrhythmic tendency. It consistently failed to provoke any arrhythmia under the control conditions (Fig. 2A; S2 extrastimulus indicated by an arrow). By contrast, provoked ventricular tachycardia (VT) was observed under hyperkalemic conditions alone (Fig. 2B). This was prevented by further hypercalcemia treatment (Fig. 2C). The incidences of provoked VT observed are summarized in Fig. 2D, demonstrating that hyperkalemia was significantly arrhythmogenic (Fisher's exact test, P<0.01), whereas hypercalcemia treatment was anti-arrhythmic under hyperkalemic conditions (Fisher's exact test, P<0.01).

View Article: PubMed Central - PubMed

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&lt;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&lt;0.05) without altering activation latencies. Endocardial APDx and VERPs were unaltered. Consequently, &#8710;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.

No MeSH data available.


Related in: MedlinePlus