Electrophysiological characteristics of myocardium after hypothermic ischemia-reperfusion in rats with different degrees of arrhythmia: an in vitro experiment

Objective To investigate the electrophysiological characteristics of myocardium after hypothermic ischemia-reperfusion (I/R) in rats with different degrees of arrhythmia using an in vitro experiment. Methods Healthy clean-grade male Sprague-Dawley rats, aged 2-3 months, weighing 300-400 g, were used in this study.The rats were sacrificed after anesthesia, and their hearts were rapidly excised.Sixteen Langendorff-perfused hearts were prepared and divided into 2 groups (n=8 each) by a random number table method: control group (group C) and hypothermic I/R group (group I/R). The hearts were made globally ischemic for 60 min followed by 30-min hypothermic (4 ℃)reperfusion to establish the model of hypothermic I/R injury.The occurrence and duration of arrhythmia and time of recovery of spontaneous heartbeat were recorded during reperfusion.The rats in group I/R were further divided into low-risk group (I/R-L group, ventricular arrhythmia score≤3 points) and high-risk group (I/R-H group, ventricular arrhythmia score>3 points) according to the arrhythmia score.Monophasic action potential amplitude (MAPA), monophasic action potential (MAP) duration at 50% and 90% repolarization (MAPD50 and MAPD90) and maximum ascending velocity (Vmax) of phase 0 in the endocardium, myocardium and epicardium of the left ventricular anterior wall were recorded at 30 min of equilibration (T0) and 15 and 30 min of reperfusion (T1, 2). The effective refractory period (ERP) and ventricular fibrillation threshold (VFT) of the left ventricle were measured by programmed electrical stimulation, and the ERP/MAPD90 ratio was calculated. Results Compared with the baseline at T0, MAPA in the three layers was significantly decreased, and MAPD50 and MAPD90 were prolonged at T1, 2 in I/R-L and I/R-H groups, and Vmax in the three layers was decreased at T1, 2 in I/R-H group (P<0.05). MAPD50 and MAPD90 in the three layers were significantly shorter at T2 than at T1 in I/R-L and I/R-H groups (P<0.05). Compared with group C, MAPD50, MAPD90 and ERP in the three layers were significantly prolonged at T1, 2, the ERP/MAPD90 ratio was decreased, and VFT was increased in I/R-L and I/R-H groups (P<0.05). Compared with I/R-L group, the duration of arrhythmia and MAPD90 and ERP in the three layers were significantly prolonged at T2, the ERP/MAPD90 ratio was decreased, and VFT was increased in group I/R-H (P<0.05). Conclusion Myocardial depolarization is inhibited, repolarization duration is prolonged, and electrophysiological stability is decreased after hypothermic I/R in the rats with arrhythmia, and the prolongation of myocardial repolarization and decrease in electrophysiological stability are more obvious in the rats at high risk of arrhythmia. Key words: Myocardial reperfusion injury; Hypothermia, induced; Arrhythmias, cardiac; Cardiac electrophysiology