Electrophysiological changes of atrial myocardium in a rat model of hypothermic ischemia-reperfusion: an in vitro experiment
10.3760/cma.j.issn.0254-1416.2019.09.014
- VernacularTitle: 低温缺血再灌注大鼠心房肌电生理变化：离体实验
- Author:
Youqin HE
1
;
Guilong WANG
1
;
Hong GAO
2
;
Yanqiu LIU
3
;
Huayu LI
1
;
Yurong FENG
1
;
Diansan SU
4
;
Jian TANG
1
Author Information
1. School of Anesthesiology, Guizhou Medical University, Guiyang 550004, China
2. The Third Affiliated Hospital of Guizhou Medical University, Duyun 558000, China
3. Department of Anesthesiology, Affiliated Hospital of Guizhou Medical University, Guizhou 550004, China
4. Department of Anesthesiology, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200127, China
- Publication Type:Journal Article
- Keywords:
Myocardial reperfusion injury;
Arrhythmias, cardiac;
Heart atria
- From:
Chinese Journal of Anesthesiology
2019;39(9):1081-1084
- CountryChina
- Language:Chinese
-
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.
