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Evaluation of the role of I_KACh in atrial fibrillation using a mouse knockout model

Pramesh Kovoor, MD, PhD^*, Kevin Wickman, PhD, Colin T. Maguire, William Pu, MD, Josef Gehrmann, MD, Charles I. Berul, MD and David E. Clapham, MD, PhD

^* Department of Cardiology, Westmead Hospital, Sydney, Australia
Department of Pharmacology, University of Minnesota, Minneapolis, Minnesota, USA
Children’s Hospital and Harvard Medical School, Boston, Massachusetts, USA

View larger version (30K): [in a new window]   Figure 1 (A) Induction of sustained atrial tachycardia in wild-type mouse after carbachol administration. Three atrial extrastimuli are delivered following a basic drive train of 150 ms. (B)Sustained atrial fibrillation, with irregular atrial cycle lengths and variable ventricular response. IECG = intracardiac electrogram; mV = millivolts; RA = right atrial; RV = right ventricular.

View larger version (28K): [in a new window]   Figure 2 Sinus node recovery times in wild-type (A) and IKACh-deficient (B) mice after pacing for 30 s at a cycle length of 150 ms. (A) The sinus node recovery times were 315 ms at baseline and 505 ms after carbachol administration. (B) The sinus node recovery times were 255 ms at baseline and 300 ms after carbachol. Pre-CCH = before administration of carbachol; Post-CCH = after administration of carbachol; RA IECG = right atrial intracardiac electrogram; RV IECG = right ventricular intracardiac electrogram.

View larger version (46K): [in a new window]   Figure 3 GIRK1 and GIRK4 are expressed in both the atrium and ventricle of the mouse. Total ribonucleic acid (RNA) from the atrium and ventricle of the adult mouse was amplified by reverse transcription-polymerase chain reaction (PCR) using primers specific for GIRK1, GIRK4 or myosin light chain (MLC)-2a. RNA from NIH-3T3 cells was used as a negative control agent, and complementary deoxyribonucleic acid (cDNA) for mouse GIRK1, GIRK4 and MLC-2a was used as a positive control agent in PCR.