七氟烷预处理改善离体大鼠心脏的再灌注心律失常

目的在Langendorff离体灌注模型研究七氟烷预处理对再灌注心律失常的影响。方法取SD大鼠心脏建立Langendorff灌注模型，随机分入以下三组：（1）对照组；（2）缺血再灌注组；（3）七氟烷预处理组（3％七氟烷预处理15分钟）。记录各组的血流动力学、心电图，测量冠脉流出液肌钙蛋白I水平，测定细胞内钙离子和活性氧水平。结果七氟烷预处理能显著增加缺血再灌注损伤后左室发展压，左室内压上升／下降速率和心率，降低左室舒张末期压力，减少冠脉流出液肌钙蛋白I水平（P均〈O．05）。在再灌注心律失常方面，与缺血再灌注组相比，七氟烷预处理能显著减少室性早搏个数从182（133）次／分降至83（52）次／分]，缩短室速41（45）s降至20（22）s]和室颤从22（43）s降至0（0）s]的发作时程，减少室颤发生率（从80％降至10％），并降低再灌注心律失常评分从4（0）降至2（O）]（P均〈0.05）。七氟烷预处理还能降低心肌细胞内钙离子和活性氧水平（P均〈0.05）。结论七氟烷预处理对缺血再灌注损伤心脏起保护作用，能改善离体大鼠心脏的再灌注心律失常。

Sevoflurane preconditioning alleviates reperfusion-induced veutricular arrhythmia in isolated rat hearts

Objective This study was designed to investigate the effects of sevoflurane preconditioning on reperfusion-induced ventricular arrhythmia in Langendorff perfused rat hearts. Methods Langendorff perfused rat hearts were randomly assigned to one of the Control, lschemiaJreperfusion and Sevoflurane preconditioning （preconditioned with 3% sevoflurane for 15 min） groups. The hemodynamics, electrocardiogram, cardiac troponin I level, intracellular calcium and reactive oxygen species levels were measured. Results Sevoflurane preconditioning significantly increased left ventricular developed pressure, maximal and minimal first derivatives of left ventricular pressure, and heart rate, reduced left ventricular end-diastolic pressure and cardiac troponin I level in I/R insulted rat hearts （all P〈0.05）. Sevoflurane preconditioning reduced the number of ventricular premature beats from 182 （133） beats/min to 83 （52） beats/min], the duration of ventrieular tachycardia from 41 （45）s to 20 （22）s] and ventricular fibrillation from 22 （43）s to 0 （0）s], the incidence of ventricular fibrillation （from 80% to 10%） , and lowered reperfusion arrhythmia score from 4 （0） to 2 （0）] compared with the ischemia/reperfusion group （all P〈0.05）. Sevoflurane preconditioning reduced intracellular calcium and reactive oxygen species levels （all P〈0.05）. Conclusions Sevoflurane preconditioning protects the hearts against ischemia/reperfusion injury and alleviates reperfusion-induced ventricular arrhythmia in isolated rat hearts.