Related Experiment Video
Updated: Jun 7, 2026

Microelectrode Array Recording of Sinoatrial Node Firing Rate to Identify Intrinsic Cardiac Pacemaking Defects in Mice
Published on: July 5, 2021
[Electrophysiological effects of antiarrhythmic drugs on pacemaker cells in guinea pig left ventricular outflow
Lan-Ping Zhao1, Li-Feng Chen, Yan-Jing Chen
1Department of Physiology, Hebei North University, Zhangjiakou 075000, China. zhaolp-doc@tom.com
Objective:
To explore the electrophysiological effects of antiarrhythmic drugs on pacemaker cells of left ventricular outflow tract.
Methods:
By using conventional intracellular microelectrode technique to record action potentials, series antiarrhythmic drugs were used to investigate the electrophysiological features and regularities of spontaneous activity of left ventricular outflow tract.
Results:
(1) Perfusion with 1 micromol/L quinidine resulted in a significant decrease in rate of pacemaker firing (RPF, P < 0.05), velocity of diastolic depolarization (VDD, P < 0.05), amplitude of action potential (APA, P < 0.05), and maximal rate of depolarization (V(max), P < 0.05), and a marked prolonging in 50% and 90% of duration of action potential (APD50 and APD90, P < 0.05). (2) 1 micromol/L lidocaine decreased RPF, VDD, MDP, APA and V(max) significantly (P < 0.05), shortened APD50 and APD90 notably (P < 0.05). (3) 1 micromol/L propafenone led to a significant decrease in RPF (P < 0.01), VDD (P < 0.05), APA (P < 0.05), V(max) (P < 0.01), and a marked prolonging in APD50 (P < 0.01) and APD90 (P < 0.05). (4) Application of 5 micromol/L propranolol resulted in a significant decrease in RPF and VDD (P < 0.01), MDP and APA (P < 0.01), V(max) (P < 0.05) and a notable prolonging in APD50 and APD90 (P < 0.05). (5) Perfusion with 1 micromol/L amiodarone resulted in a significant decrease in RPF and VDD (P < 0.01), APA (P < 0.01), V(max) (P < 0.05), a marked prolonging in APD50 (P < 0.01) and APD90 (P < 0.05). (6) 1 micromol/L verapamil significantly decreased RPF and VDD (P < 0.01), MDP and APA (P < 0.05), V(max) (P < 0.05), notably prolonged APD50 and APD90 (P < 0.01). (7) 50 micromol/L adenosine significantly decreased RPF and VDD (P < 0.05), APA (P < 0.05), V(max) (P < 0.01), markedly shortened APD50 and APD90 (P < 0.05).
Conclusion:
All kinds of antiarrhythmic drugs can decrease the autorhythmicity of guinea pig left ventricular outflow tract. By altering APD50 and APD90, they can affect effective refractory period (ERP) and having a significant effect on autorhythmicity of left ventricular outflow tract.
Related Concept Videos
Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers
Class 1A Antiarrhythmic Drugs: These drugs work by moderately blocking sodium channels,...
Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers
Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers
Mechanism of Cardiac Arrhythmias
Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers
Verapamil, a calcium channel blocker, inhibits calcium movement across myocardial cell membranes and vascular smooth muscle. This results in the dilation of coronary and...
Dysrhythmias VI: Management of Dysrhythmias
