Background: The mechanism underlying the occurrence of the J wave in low temperature remains unclear. However, low temperature is associated with metabolic disorder and 5' AMP-activated protein kinase (AMPK), which modulates ionic currents and cardiac metabolism. This study investigated whether AMPK regulation can modulate the occurrence of the J wave at low temperature. Methods: Unipolar and bipolar leads were used to record monophasic action potential (the endocardium and epicardium) and pseudo-electrocardiograms (inferior leads) to study the cardiac electrical activity. Measurements were taken in isolated Langendorff rabbit hearts at both 30℃ and 37℃ before and after administration of 4-aminopyridine (an ultrarapid delayed rectifier potassium current inhibitor, IKur, 50 µmol L−1), PF06409577 (an AMPK activator, 1 µmol L−1), compound C (an AMPK inhibitor, 10 µmol L−1) and glibenclamide (an ATP-sensitive inward rectifier potassium channel inhibitor, IKATP, 20 µmol L−1). Results: The amplitude of the J wave (2.46 ± 0.34 mV vs. 1.11 ± 0.23 mV, P <.01) at 30℃ (n = 15) was larger than that at 37℃ (n = 15). PF06409577 (1 µmol L−1) increased the J waves at both 30℃ and 37℃. In contrast, compound C (10 µmol L−1) reduced J wave at both 37℃ and 30℃. Low-temperature-induced J waves were individually suppressed by 4-AP (50 µmol L−1) and glibenclamide (20 µmol L−1). Conclusions: AMPK inhibition reduces low-temperature-induced J waves and possible ventricular arrhythmogenesis by modulating IKATP and IKur channels.
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