Influence of apamin on the extracellularly recorded action potentials profiles of subepicardial cardiomyocytes of the rat heart in myocardial infarction

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Abstract

The role of small-conductance Ca²⁺-activated K⁺-channels (SK channels) in the pathogenesis of cardiomyopathies of various etiologies remains poorly understood. The purpose of this work was to evaluate the effect of the blocker of SK channels, apamin, on the extracellularly recorded action potentials (eAPs) of subepicardial myocytes in the left ventricles of sham-operated rats and rats with myocardial infarction caused by ischemia-reperfusion. It was found that local delivery of the SK channel blocker apamin at a concentration of 500 nM to the eAP recording area did not affect the eAP profiles in the group of sham-operated rats but caused a significant slowdown in the repolarization time and a decrease in the afterhyperpolarization phase of eAPs in the group of rats with myocardial infarction. These data suggest that changes in the waveform of eAPs after infarction are associated with increased expression and/or activity of SK channels in subepicardial myocytes. The possible role of these channels in the structural and functional remodeling of the myocardium of the left ventricle of the heart after ischemia-reperfusion is discussed.

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A. V. Stepanov

Sechenov Institute of Evolutionary Physiology and Biochemistry of the Russian Academy of Sciences

Author for correspondence.
Email: botanik2407@gmail.com
Russian Federation, Saint Petersburg

M. G. Dobretsov

Sechenov Institute of Evolutionary Physiology and Biochemistry of the Russian Academy of Sciences

Email: botanik2407@gmail.com
Russian Federation, Saint Petersburg

Yu. A. Filippov

Sechenov Institute of Evolutionary Physiology and Biochemistry of the Russian Academy of Sciences

Email: botanik2407@gmail.com
Russian Federation, Saint Petersburg

I. V. Kubasov

Sechenov Institute of Evolutionary Physiology and Biochemistry of the Russian Academy of Sciences

Email: botanik2407@gmail.com
Russian Federation, Saint Petersburg

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2. Fig. 1. Averaged QRST complexes of LO (a) and IR (b) rats in standard lead II and average values ​​of the amplitudes of the Q, R, S, T waves (c) for the entire sample 4 weeks after surgery (red columns – LO group (15 rats); blue columns – IR group (21 rats).

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3. Fig. 2. Sections of the hearts of LO- (a) and IR-rats (b), stained with a solution of triphenyltetrazolium chloride. The dotted line indicates the boundaries of scar tissue.

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4. Fig. 3. Representative examples of the eAP1 and eAP2 profiles of the LV subepicardium in rats of the LO- (a) and IR-groups (b). All responses are normalized to the value of their first and only negative peak for eAP1 (P1); P2 is the mark of the second negative peak in eAP2. The arrows indicate the AHP phase (afterhyperpolarization).

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5. Fig. 4. Apamin does not affect the decline in the 1st and 2nd type of LV epicardial myocytes in the heart of LO rats.

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6. Fig. 5. Apamin modulates the decline in ePP of type 1 and 2 epicardial myocytes of the left ventricle of the heart of IR-group rats.

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