Abstract: Objective: To observe the effects of hypothermia on the repolarization duration and the expression of Kir2.1 protein of ventricular myocytes in isolated rat heart and explore the role of Kir2.1 protein.Methods: Eighteen healthy adult male Sprague-Dawley rats were randomly divided into three groups (n=6 per group): Control group (C group), 35℃ group (H₁ group), 32℃ group (H₂ group). Langendorff isolated heart models were established. After 15 min 37℃ K-H fluid banlanced perfusion, C group continued to perfuse the K-H solution at 37℃ for 30 minutes, H₁ group continued to perfuse the K-H solution at 35℃ for 30 minutes, H₂ group continued to perfuse the K-H solution at 32℃ for 30 minutes. At 15 min of balanced perfusion (T₁), and 30 min of continuous perfusion (T₂), the heart rate,and the MAP in the three layers of the left ventricular anterior wall were recorded, the action potential duration at 50% repolarization (MAPD₅₀), the action potential duration at 90% repolarization (MAPD₉₀) and transmural dispersion of repolarization(TDR) were calculated. At the same time, the occurrence of arrhythmia was recorded. The expression of Kir2.1 protein was measured by Western blot. The average optical density (AOD) and the distribution of Kir2.1 protein were measured by immunohistochemistry in the ventricular tissue measured by electrophysiology. Results: Compared with T₀, the heart rate was decreased, MAPD₅₀ and MAPD₉₀ were prolonged significantly (P＜0.05), and TDR was increased significantly (P＜0.05) in H₁ group, H₂ group at T₁. Compared with C group, the HR was decreased, the MAPD₉₀ was prolonged significantly (P＜0.05), TDR was increased significantly (P＜0.05),the expression and the AOD of Kir2.1 protein were decreased significantly (P＜0.05) in H₁group, H₂group at T₁. Compared with H₁ group, the heart rate of H₂ group was decreased significantly (P＜0.05), MAPD₅₀ and MAPD₉₀ were prolonged significantly (P＜0.05), and TDR was increased significantly (P＜0.05) at T₁. The distribution of Kir2.1 protein in group C was normal, while the distribution of Kir2.1 in H₁ group and H₂ group was disordered. Conclusion: Hypothermia prolonged the ventricular duration of repolarization and increased the dispersion of repolarization. The mechanism is related to the down-regulation the expression of Kir2.1 protein and the disorder of the distribution of Kir2.1 protein.

Key words: hypothermia, monophasic action potential, transmural dispersion of repolarization, arrhythmia, Kir2.1, electrophysiological techniques