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目的:探讨阿托伐他汀对急性心肌梗死后室性心律失常的抑制作用及机制。方法:45只雄性急性心肌梗死大鼠随机均分为高、低剂量阿托伐他汀组及急性心肌梗死组(每组15只)。另取10只大鼠作为假手术组。高、低剂量阿托伐他汀组每日分别给予阿托伐他汀10mg·kg-1·d-1、20mg·kg-1·d-1灌胃1周,假手术组和急性心肌梗死对照组不予治疗。第1周末以程序电刺激诱发各组大鼠室性心律失常后,假手术组取位于左心室游离壁心肌组织,心肌梗死各组取位于左心室梗死边缘带心肌组织检测白细胞介素(IL)-8表达。结果:急性心肌梗死组梗死边缘带IL-8表达水平及室性心律失常诱发率均高于假手术组(P<0.01),低剂量阿托伐他汀组梗死边缘带IL-8表达水平及室性心律失常诱发率显著低于急性心肌梗死组(P<0.05)。高剂量阿托伐他汀组梗死边缘带IL-8表达水平及室性心律失常诱发率显著低于低剂量组(P<0.05)。结论:阿托伐他汀可能通过抑制IL-8过度表达来降低室性心律失常发生率,其作用呈剂量依赖性。
Objective: To investigate the inhibitory effect of atorvastatin on ventricular arrhythmia after acute myocardial infarction and its mechanism. Methods: Forty five male rats with acute myocardial infarction were randomly divided into high and low dose atorvastatin group and acute myocardial infarction group (15 rats in each group). Another 10 rats as sham group. High-dose and low-dose atorvastatin groups were given daily atorvastatin 10mg · kg-1 · d-1 and 20mg · kg-1 · d-1 for 1 week, sham operation group and acute myocardial infarction control group No treatment. After the first week of program induced by electrical stimulation of ventricular arrhythmias in each group, the sham operation group was located in the left ventricular free wall myocardial tissue, myocardial infarction in each group taken at the margin of left ventricular infarction with myocardial tissue detection of interleukin (IL) -8 expression. Results: The expression of IL-8 in the marginal zone of infarction and induction rate of ventricular arrhythmia in acute myocardial infarction group were significantly higher than those in sham operation group (P <0.01). The expression of IL-8 in infarct zone of low dose atorvastatin group and The induction rate of arrhythmia was significantly lower than that of acute myocardial infarction group (P <0.05). The level of IL-8 in the marginal zone of infarction and induction rate of ventricular arrhythmia in high dose atorvastatin group were significantly lower than those in low dose group (P <0.05). Conclusion: Atorvastatin may reduce the incidence of ventricular arrhythmias by inhibiting the over-expression of IL-8 in a dose-dependent manner.