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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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(A) Epicardial and (B) endocardial activation latency obtained under control conditions, hyperkalemia alone or following hypercalcemia treatment (n=7). These values were not altered by hyperkalemia alone or following hypercalcemia treatment (analysis of variance, P>0.05).
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f6-br-0-0-735: (A) Epicardial and (B) endocardial activation latency obtained under control conditions, hyperkalemia alone or following hypercalcemia treatment (n=7). These values were not altered by hyperkalemia alone or following hypercalcemia treatment (analysis of variance, P>0.05).

Mentions: Hyperkalemia is known to cause prolongations in QRS durations, reflecting slowed ventricular conduction in humans (6). Reduced CVs have been shown to be an important factor in producing ventricular arrhythmogenesis following heptanol treatment (31). Therefore, in the studythe activation latencies, which provide an indication of the CVs, were quantified to determine whether changes in these values contribute to the arrhythmogenic substrate. Epicardial and endocardial activation latencies had values of 16.7±0.8 (Fig. 6A) and 17.0±1.1 msec (Fig. 6B), respectively, under normokalemic conditions. These values were not altered by hyperkalemia alone or following hypercalcemia treatment (ANOVA, P>0.05). Epicardial activation latencies were not significantly different from their corresponding endocardial activation latencies under any of the aforementioned pharmacological conditions studied (P>0.05).


Anti-arrhythmic effects of hypercalcemia in hyperkalemic, Langendorff-perfused mouse hearts
(A) Epicardial and (B) endocardial activation latency obtained under control conditions, hyperkalemia alone or following hypercalcemia treatment (n=7). These values were not altered by hyperkalemia alone or following hypercalcemia treatment (analysis of variance, P>0.05).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f6-br-0-0-735: (A) Epicardial and (B) endocardial activation latency obtained under control conditions, hyperkalemia alone or following hypercalcemia treatment (n=7). These values were not altered by hyperkalemia alone or following hypercalcemia treatment (analysis of variance, P>0.05).
Mentions: Hyperkalemia is known to cause prolongations in QRS durations, reflecting slowed ventricular conduction in humans (6). Reduced CVs have been shown to be an important factor in producing ventricular arrhythmogenesis following heptanol treatment (31). Therefore, in the studythe activation latencies, which provide an indication of the CVs, were quantified to determine whether changes in these values contribute to the arrhythmogenic substrate. Epicardial and endocardial activation latencies had values of 16.7±0.8 (Fig. 6A) and 17.0±1.1 msec (Fig. 6B), respectively, under normokalemic conditions. These values were not altered by hyperkalemia alone or following hypercalcemia treatment (ANOVA, P>0.05). Epicardial activation latencies were not significantly different from their corresponding endocardial activation latencies under any of the aforementioned pharmacological conditions studied (P>0.05).

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