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| 七氟醚对低温全心缺血-再灌注心脏电传导及Cx43 Ser368磷酸化的影响 |
| Effect of sevoflurane on the electrical conduction and the phosphorylation of Cx43 Ser368 in the heart of hypothermic global ischemia-reperfusion |
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| DOI：10.12089/jca.2020.12.016 |
| 中文关键词: 七氟醚 缺血-再灌注 电传导 缝隙连接蛋白43 |
| 英文关键词: Sevoflurane Ischemia-reperfusion Electrical conduction Connexin 43 |
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| 中文摘要: |
目的 观察七氟醚对低温全心缺血-再灌注心室肌电传导及Cx43 Ser368磷酸化的影响。
方法 制备成功的离体灌注工作心脏24只，随机分为三组：对照组（C组）、低温全心缺血-再灌注组（IR组）和1.0 MAC七氟醚处理组（Sev组），每组8只。C组：37 ℃ K-H液平衡灌注15 min后继续灌注37 ℃ K-H液105 min；IR组：37 ℃ K-H液平衡灌注15 min后继续灌注37 ℃ K-H液15 min，注射Thomas液（4 ℃，20 ml/kg）使心脏停搏60 min，4 ℃ K-H液保护心脏，停搏30 min时半量复灌Thomas液（4 ℃，10 ml/kg），60 min时使用37 ℃ K-H液再灌注30 min；Sev组：37 ℃ K-H液平衡灌注15 min后继续灌注含饱和1.0 MAC七氟醚的37 ℃ K-H液15 min，注射Thomas液（4 ℃，20 ml/kg）使心脏停搏60 min，4 ℃ K-H液保护心脏，停搏30 min时半量复灌Thomas液（4 ℃，10 ml/kg），60 min时使用含饱和1.0 MAC七氟醚的37 ℃ K-H液再灌注30 min。于再灌注即刻至灌注结束，记录离体心脏复跳时间（再灌注即刻至心脏首次跳动所需的时间），室性心律失常（室性早搏、室性心动过速、室性颤动）发生情况和持续时间。采用心脏刺激仪行程控刺激，测定并记录有效不应期（ERP）、传导速度(CV）。采用免疫印迹法检测心室肌组织Cx43和Cx43 Ser368蛋白相对含量。
结果 与C组比较，IR组和Sev组ERP明显延长，CV明显减慢（P＜0.05）；IR组Cx43及Cx43 Ser368蛋白相对含量明显降低（P＜0.05）。与IR组比较，Sev组心脏复跳时间明显缩短，心律失常发生率明显降低，心律失常持续时间明显缩短，ERP明显缩短，CV明显增快，Cx43及Cx43 Ser368蛋白相对含量明显升高（P＜0.05）。
结论 七氟醚可以上调低温全心缺血-再灌注心室肌组织Cx43和Cx43 Ser368的表达，促使心室肌电传导增快、有效不应期缩短，降低再灌注心律失常的发生。 |
| 英文摘要: |
Objective To observe the effect of sevoflurane on the electrical conduction and the phosphorylation of Cx43 Ser368 on the heart of hypothermic global ischemia-reperfusion.
Methods Twenty-four isolated perfused working hearts were randomly divided into 3 groups (n = 8 in each): control group (group C), hypothermia global ischemia-reperfusion group (group IR), and 1.0 MAC sevoflurane group (group Sev). In group C, the heart was perfused with 37 ℃ K-H solution for 15 minutes and then perfused with 37 ℃ K-H solution for 105 minutes. In group IR, the heart was perfused with 37 ℃ K-H solution for 15 minutes and then perfused with 37 ℃ K-H solution for 15 minutes. Thomas solution (4 ℃, 20 ml/kg) was injected to make the heart stop beating for 60 minutes, and the surrounding of the heart was protected by 4 ℃ K-H solution, and Thomas solution (4 ℃, 10 ml/kg) was refilled when the heart stopped for 30 minutes. In group Sev, the heart was perfused with 37 ℃ K-H solution for 15 minutes and then perfused with 37 ℃ K-H solution containing 1.0 MAC sevoflurane for 15 minutes. Thomas solution (4 ℃, 20 ml/kg) was injected to stop the heart beating for 60 minutes, and the surrounding of the heart was protected by 4 ℃ K-H solution. Thomas solution (4 ℃, 10 ml/kg) was refilled for 30 minutes, and 37 ℃ K-H solution containing 1.0 MAC sevoflurane was used for 30 minutes. From the instance to the end of reperfusion time, the rebeating time (the time from reperfusion to the first beating) of isolated heart was recorded, the number and duration of ventricular arrhythmias (ventricular premature beat, ventricular tachycardia and ventricular fibrillation) were recorded. The effective refractory period (ERP) and conduction velocity (CV) were measured and recorded from programmed electrical stimulation by cardiac stimulator. The relative content of Cx43 and Cx43 ser368 protein in ventricular tissue were detected by Western blot.
Results Compared with group C, ERP was significantly prolonged, and CV was significantly slowed in group IR and group Sev, the expression of Cx43 and Cx43 ser368 protein decreased in group IR (P < 0.05). Compared with group IR, the cardiac rebeating time was significantly shorter, the incidence of arrhythmia was significantly decreased, the ERP was significantly shorter, the CV was significantly faster, and the protein content of Cx43 and Cx43 ser368 were significantly higher in group Sev (P < 0.05).
Conclusion Sevoflurane may upregulate the expression of Cx43 and Cx43 ser368 in the ventricular tissue of hypothermic global ischemia-reperfusion, accelerate CV and decrease ERP, so as to reduce the incidence of reperfusion arrhythmia. |
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