Electrophysiological changes of atrial myocardium in a rat model of hypothermic ischemia-reperfusion: an in vitro experiment / 中华麻醉学杂志

ABSTRACT

Objective To evaluate the electrophysiological changes of atrial myocardium in a rat model of hypothermic ischemia-reperfusion (I/R).Methods Sixteen isolated Sprague-Dawley rat hearts successfully perfused in the Langendorff apparatus were divided into control group (group C) and hypothermic I/R group (group IR) using a random number table method,with 8 heats in each group.Heats in group IR were further divided into reperfusion-non-atrial arrhythmia subgroup (group R-NAA) and reperfusion-atrial arrhythmia subgroup (group R-AA) depending on whether atrial arrhythmia occurred after reperfusion.In group C,the heart was perfused with K-H solution at 37 ℃ for 120 min.In group IR,the heart was perfused with K-H solution at 37 ℃ for 30 min and then perfusion was stopped,cardiac arrest was induced for 60 min through injecting Thomas solution (4 ℃,20 ml/kg),the area around the heart was protected with low temperature (4 ℃℃) Thomas solution,and hearts were resuscitated with 4 ℃ Thomas solution (10 ml/kg) at 30 min after cardiac arrest and with 37 ℃ K-H solution for 30 min staring from 60 min after cardiac arrest.At 30 min of equilibration (T0),105 min of equilibration/15 min of reperfusion (T1),and 120 min of equilibration/30 min of reperfusion (T2),right atrial monophasic action potentials,maximal velocity of phase zero,monophasic action potential amplitude (MAPA) and MAP duration at 50％ and 90％ of repolarization (MAPDs0and MAPDg0) were measured.Right-atrium conduction velocity and effective refractory period were recorded at T2,and the ratio of ERP to MAPD90 (ERP/MAPD90) was calculated.Atrial fibrillation was induced by programmed electrical stimulation,and the maximum pacing cycle length of inducing atrial fibrillation (AF-PCLm=) was recorded.Results Compared with C and R-NAA groups,the maximal velocity of phase zero was significantly decreased and MAPDg0 was increased at T1,the right-atrium conduction velocity and ERP/MAPDg0 ratio were decreased and MAPD90,effective refractory period and AF-PCLmax were increased at T2 in group R-AA (P＜ 0.05).Conclusion The decrease in depolarization velocity,prolongation of repolarization duration and decrease in conduction velocity,excitability and electrical stability may be the electrophysiological mechanism of reperfused atrial arrhythmia in rats.