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. Author manuscript; available in PMC: 2013 Sep 1.
Published in final edited form as: J Mol Cell Cardiol. 2012 May 25;53(3):350–353. doi: 10.1016/j.yjmcc.2012.05.010

Figure 1. Atrial KCNE1 downregulation in porcine postoperative atrial fibrillation.

Figure 1

A. Representative tracings of ECG, right ventricular pressure (RVP), systemic arterial pressure (AP), and pulmonary arterial pressure (PAP) during atrial pacing at a rate of 80/min and following induction of AF

B. Incidence of sustained AF in Control and 3-days postoperative pigs. *P=0.0079 versus Controls

C. Left atrial effective refractory period duration versus incidence of AF sustained >60 s after 10 s rapid pacing (Y, yes versus N, no) plotted for control and 3-days postoperative pigs as indicated

D. Mean KCNE1 transcript intensity in LA tissue of Control (C) and postoperative (P) pigs; n = 3–5

E. Mean GAPDH transcript intensity in LA tissue of Control (C) and postoperative (P) pigs; n = 3–5

F. Left, exemplar western blots using anti-KCNE1 antibody to probe lysates from LA tissue of Control (C) and postoperative (P) pigs; right, band densitometry for blots as in left; n = 4–5, each performed in triplicate

G. Left, exemplar western blots using anti-GAPDH antibody to probe lysates from LA tissue of Control (C) and postoperative (P) pigs; right, band densitometry for blots as in left; n = 4–5, each performed in triplicate

H. Hypothetical framework of POAF etiology drawing from the findings herein and previous functional analyses of the genes listed.