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<!DOCTYPE article PUBLIC "-//NLM//DTD JATS (Z39.96) Journal Publishing DTD v1.2d1 20170631//EN" "JATS-journalpublishing1.dtd">
      <Volume-Issue>Volume 4, Issue 3</Volume-Issue>
      <Season>January - March 2014</Season>
      <Abstract>Background and Objectives: In amphibian ventricle, steady loss of calcium occurs during diastole. Sodium calcium exchanger (NCX) clears calcium to the exterior causing rhythm generation. Calcium loss was demonstrated by decrease in the contractile force after an imposed rest  period‑rest  induced  decay  (RID).  Calcium  channel blockers  with  anti‑arrhythmic  activity  cause  increase  in contractile force following a rest period (rest induced potentiation), which could be due to reversal of NCX. Hence other therapeutically used anti‑arrhythmic agents may also influence the working direction of NCX. Materials and Methods: Frog ventricular strips when electrically stimulated in solution resembling extracellular fluid show a steady state of contraction. Different classes of anti‑arrhythmic  agents  according  to  Vaugan  William’s classification belonging to classes Ia, Ib, III and IV were examined for reversal of NCX. Rest periods were imposed in between contraction, ranging from 20 to 100 and 180 s and similar protocol was followed with the drug   of intervention on the same tissue. The post rest and pre rest amplitudes of contraction were compared and analysed. Results: RID that was observed with the control solution did not get converted into potentiation with any of the above mentioned classes of anti‑arrhythmic agents. Interpretation and Conclusion: Unlike the results observed with calcium channel blockers verapamil and diltiazem, no reversal in the direction of the working mode of NCX was noted with the above said anti‑arrhythmic agents as shown by  the  persistence  of  RID.  Hence  these  anti‑arrhythmic agents do not influence the working mode of NCX in their anti‑arrhythmic action.</Abstract>
      <Keywords>Anti‑arrhythmic,    Calcium,    Sodium calcium exchanger, Rest induced decay, Rest induced potentiation</Keywords>
        <Abstract>https://njbms.in/ubijournal-v1copy/journals/abstract.php?article_id=1527&amp;title=EFFECT OF ANTI‑ARRHYTHMIC AGENTS ON SODIUM CALCIUMEXCHANGER IN THE FROG HEART</Abstract>