Related Experiment Video

Updated: Sep 20, 2026

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
10:53

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents

Published on: July 3, 2013

Adriamycin-induced alterations of the action potential in rat papillary muscle

M L Lazarus, K L Rossner, K M Anderson

    Cardiovascular Research
    |August 1, 1980
    PubMed

    Insights

    Adriamycin (ADR) prolongs cardiac action potential duration by altering myocardial ion channel conductance, not by depressing cell metabolism. This study reveals ADR

    Area of Science:

    • Cardiology
    • Pharmacology
    • Electrophysiology

    Background:

    • Adriamycin (ADR) is a widely used chemotherapy agent.
    • Cardiotoxicity is a significant side effect of ADR treatment.
    • The precise electrophysiological mechanisms underlying ADR-induced cardiotoxicity require further elucidation.

    Purpose of the Study:

    • To investigate the effects of adriamycin on the electrophysiological properties of the myocardium.
    • To determine the impact of ADR on cardiac action potential parameters.
    • To explore the potential mechanisms responsible for ADR's electrophysiological effects.

    Main Methods:

    • Intracellular recordings of cardiac action potentials in rat papillary muscles.
    • In vivo administration of ADR (20 mg/kg single dose or 5 mg/kg x 4 days).
    • In vitro superfusion of papillary muscles with ADR (200 µmol/L).

    Main Results:

    • Adriamycin significantly prolonged the duration of the cardiac action potential at 20%, 50%, and 98% repolarization.
    • ADR did not depress myocardial cell metabolism, as indicated by unchanged action potential duration with metabolic inhibitors (NaCN, dinitrophenol).
    • Upstroke velocity, reflecting sodium conductance, remained unaltered, suggesting ADR affects calcium and/or potassium conductance.

    Conclusions:

    • Adriamycin alters myocardial electrophysiology primarily by prolonging action potential duration.
    • The mechanism does not involve metabolic depression but likely affects ion channel function (calcium and/or potassium).
    • Further research is needed to identify the specific ion channels and molecular pathways involved in ADR-induced electrophysiological changes.

    More Related Videos

    Contractility Measurements on Isolated Papillary Muscles for the Investigation of Cardiac Inotropy in Mice06:22

    Contractility Measurements on Isolated Papillary Muscles for the Investigation of Cardiac Inotropy in Mice

    Published on: September 17, 2015

    Laser-Induced Action Potential-Like Measurements of Cardiomyocytes on Microelectrode Arrays for Increased Predictivity of Safety Pharmacology10:41

    Laser-Induced Action Potential-Like Measurements of Cardiomyocytes on Microelectrode Arrays for Increased Predictivity of Safety Pharmacology

    Published on: September 13, 2022

    Related Concept Videos

    G-Protein Gated Ion Channels01:21

    G-Protein Gated Ion Channels

    GPCRs are primarily responsible for our sense of smell, taste, and vision.  The binding of a sensory stimulus activates GPCR to stimulate effector proteins, many of which are ion channels in the sensory organs. GPCRs modulate the opening and closing of the target ion channels either directly by binding them, or by releasing second messengers that activate these channels. As ions move across the membrane, the membrane potential is altered, which induces an appropriate response.
    Sensory organs,...
    Antihypertensive Drugs: Action of Calcium Channel Blockers01:18

    Antihypertensive Drugs: Action of Calcium Channel Blockers

    Calcium ions are essential to contract smooth muscle cells in blood vessels. They enter these cells through voltage-dependent calcium channels, specifically L-type calcium channels in the cell membrane. These L-type calcium channels are integral to the excitation-contraction coupling process in smooth muscle. When a stimulus is received by smooth muscle cells, their membrane depolarizes. This alteration in membrane potential instigates the opening of L-type calcium channels. As a result,...
    Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers01:22

    Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

    Class I antiarrhythmic drugs are used to treat various types of arrhythmias or irregular heart rhythms. These drugs block the sodium (Na+) channels in the cardiac cells, thereby affecting the movement of electrical impulses across the heart. Class I antiarrhythmic drugs are divided into three subgroups: Class IA, Class IB, and Class IC, each with distinct mechanisms of action and effects on the heart.
    Class 1A Antiarrhythmic Drugs: These drugs work by moderately blocking sodium channels,...
    Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers01:24

    Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers

    Adrenergic stimulation generally impacts cardiac rate and rhythm. Specifically, stimulation of the β-adrenoceptors triggers an increase in intracellular calcium ion influx and pacemaker currents, which may cause arrhythmias. Catecholamines like adrenaline also demonstrate β2-adrenoceptor-mediated hypokalemia, impacting cardiac action potential and disrupting the normal cardiac rhythm. Class II antiarrhythmic drugs are β-adrenoceptor antagonists or β-blockers, which indirectly block calcium...