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 (MAPD50 and MAPD90) 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-PCLmax) was recorded.@*Results@#Compared with C and R-NAA groups, the maximal velocity of phase zero was significantly decreased and MAPD90 was increased at T1, the right-atrium conduction velocity and ERP/MAPD90 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.