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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.

No MeSH data available.


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Representative epicardial MAP recordings obtained under (A) control conditions, (B) hyperkalemia alone or (C) following hypercalcemia treatment during regular 8 Hz pacing. Typical regular rhythms can be observed, with each MAP occurring directly following its preceding stimulus. MAP, monophasic action potential.
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f1-br-0-0-735: Representative epicardial MAP recordings obtained under (A) control conditions, (B) hyperkalemia alone or (C) following hypercalcemia treatment during regular 8 Hz pacing. Typical regular rhythms can be observed, with each MAP occurring directly following its preceding stimulus. MAP, monophasic action potential.

Mentions: 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. Fig. 1 shows representative traces of epicardial MAP recordings under these pharmacological conditions, in which stable MAPs occurring directly following its preceding stimulus, with consistent waveforms, can be observed.


Anti-arrhythmic effects of hypercalcemia in hyperkalemic, Langendorff-perfused mouse hearts
Representative epicardial MAP recordings obtained under (A) control conditions, (B) hyperkalemia alone or (C) following hypercalcemia treatment during regular 8 Hz pacing. Typical regular rhythms can be observed, with each MAP occurring directly following its preceding stimulus. MAP, monophasic action potential.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f1-br-0-0-735: Representative epicardial MAP recordings obtained under (A) control conditions, (B) hyperkalemia alone or (C) following hypercalcemia treatment during regular 8 Hz pacing. Typical regular rhythms can be observed, with each MAP occurring directly following its preceding stimulus. MAP, monophasic action potential.
Mentions: 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. Fig. 1 shows representative traces of epicardial MAP recordings under these pharmacological conditions, in which stable MAPs occurring directly following its preceding stimulus, with consistent waveforms, can be observed.

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<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.

No MeSH data available.


Related in: MedlinePlus