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(Circulation. 1996;94:2641-2648.)
© 1996 American Heart Association, Inc.


Articles

In Vivo Cardiac Electrophysiology Studies in the Mouse

Charles I. Berul, MD; Mark J. Aronovitz; Paul J. Wang, MD; Michael E. Mendelsohn, MD

the Divisions of Pediatric Cardiology (C.I.B.) and Cardiology (M.J.A., P.J.W., M.E.M.) and the Molecular Cardiology Research Center (C.I.B., M.E.M.), New England Medical Center and Tufts University School of Medicine, Boston, Mass.

Correspondence to Charles I. Berul, MD, or Michael E. Mendelsohn, MD, Molecular Cardiology Research Center, Tufts–New England Medical Center, Box 80, 750 Washington St, Boston, MA 02111.

Background This report describes a novel in vivo mouse epicardial cardiac electrophysiology study based on clinical protocols used to evaluate cardiac conduction in human patients. The technique allows extensive electrophysiological evaluation, including the response to pacing, programmed stimulation, and pharmacological agents.

Methods and Results Surface six-lead ECG data from 18 C57BL/6J mice are presented. Normal cardiac conduction properties for 14 of 18 mice that underwent the procedure are summarized, including determination of sinus node recovery times, AV conduction properties, and atrial, AV, and ventricular effective refractory periods. A subset of six mice was studied after the administration of either procainamide (n=3) or quinidine (n=3). All animals in the procainamide group developed either second-degree or complete AV block spontaneously. The sinus cycle length and refractory periods prolonged on procainamide or quinidine, but no tachyarrhythmias could be induced with atrial or ventricular programmed stimulation.

Conclusions This mouse electrophysiology method allows rapid assessment of the conduction properties of the murine heart. The ability to analyze cardiac conduction in normal and transgenic mice provides a powerful tool for examining molecular electrophysiological mechanisms in normal physiology and disease states.


Key Words: electrophysiology • mice • genes • arrhythmia




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