Effect and mechanism of dexmedetomidine on ischemic arrhythmia

Objective: To explore the antiarrhythmic effect and mechanism of dexmedetomidine, a myocardial α2 receptor agonist in vitro. Methods: Fifty Wistar rats were randomly divided into five groups (n = 10): sham operation group (Ctl), arrhythmia model group (Model), arrhythmia + dexmedetomidine group (Dex), arrhythmia + yohimbine + dexmedetomidine group (Yoh + Dex), arrhythmia + yohimbine group (Yoh). The Ctl group just thread left anterior descending coronary artery without ligation. Model group recorded 10 minutes of normal ECG, ligated the left anterior descending coronary artery, and continued to record the ECG for 2 hours. Dex group, Yoh + Dex group and Yoh group were ligated left anterior descending coronary artery after administration. Use BL-420E system to record ECG; Curtis and Walker arrhythmia scores were used to analyze the severity of arrhythmia; perform survival analysis according to the life span of each group of rats; after 21 days of modeling, measure the area of myocardial infarction by TTC staining. The pH value of extracellular fluid was decreased to simulate myocardial ischemia. Patch clamp technique was used to detect the action potential duration of myocardial cells. Results: Compared with the Ctl group, the arrhythmia score and myocardial infarction area in the Model group was increased (P < 0.05), the mortality and myocardial infarction area were alsosignificantly reduced (P < 0.05). Compared with Model group and Yoh group, the arrhythmia score of Dex group was significantly lower (P < 0.001), the mortality and myocardial infarction area were significantly lower (P < 0.05); Dexmedetomidine shortened QTc interval (P < 0.01), APD50 and APD90 (P < 0.05). The 2 receptor blocker Yohimbine inhibited the effect of dexmedetomidine. Conclusion: Dexmedetomidine affects the action potential repolarization process by stimulating myocardial 2 receptors, and prevents ischemia-induced ventricular arrhythmia.