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目的探索肾交感神经消融对心肌梗死(MI)后室性心律失常的影响以及可能机制。方法将18只成年杂种犬随机分为假手术(SO)组、MI组、和肾交感神经消融加MI(RD+MI,肾交感神经消融:选用3.5 mm消融电极,6~8W消融60s)组,每组6只。记录各组MI后1 h内心电图(SO组,暴露双侧肾动脉后记录心电图1 h);记录左侧星状神经节(LSG)活性(SO组:记录心电图1 h后记录LSG活性;MI组和RD+MI组:记录MI后LSG活性);测量各组心肌组织内组胺、5羟色胺(5-HT)、丙二醛(MDA)和超氧化物歧化酶(SOD)的表达。结果 SO组无室性心律失常事件的发生。与MI组比较,RD+MI组中1 h内室性心律失常事件{单发室早[(35±6.7)个vs(87±24)个,P<0.05]、成对室早[(14±7.3)个vs(26±10)个,P<0.05]、室性心动过速[(2.1±1.3)次vs(6.3±2.4)次,P<0.05]}发生、LSG活性、心肌组织组胺[(8.70±1.46)ng/ml vs(15.66±1.74)ng/ml,P<0.05]、5-HT[(51.79±5.95)ng/ml vs(63.24±10.21)ng/ml,P<0.05]表达水平和氧化应激水平{MDA[(2.47±0.50)nmol/mg vs(4.36±0.98)nmol/mg,P<0.05]表达降低,SOD[(502.22±66.35)U/mg vs(392.15±33.33)U/mg,P<0.05]表达增加}均明显降低。结论 RD可显著抑制MI中心脏神经活性的增加和心律失常事件发生,其机制可能与抑制心肌组织组胺、5-HT和氧化应激水平有关。
Objective To explore the effects of renal sympathetic ablation on ventricular arrhythmias after myocardial infarction (MI) and its possible mechanism. Methods 18 adult mongrel dogs were randomly divided into sham operation (SO) group, MI group, and renal sympathetic ablation plus MI (RD + MI, renal sympathetic nerve ablation: 3.5mm ablation electrode, 6 ~ 8W ablation 60s) , 6 in each group. The electrocardiogram (SO group, 1 h after electrocardiography was recorded) was recorded within 1 h after MI. Left stellate ganglion (LSG) activity was recorded (SO group: LSG activity was recorded 1 h after electrocardiogram recording; MI Group and RD + MI group: LSG activity was recorded after MI). The expression of histamine, serotonin (5-HT), malondialdehyde (MDA) and superoxide dismutase (SOD) were measured in each group. Results SO group no ventricular arrhythmia occurred. Compared with the MI group, the incidence of ventricular arrhythmia within 1 h in RD + MI group was (35 ± 6.7) vs 87 ± 24 (P <0.05) ± 7.3) vs (26 ± 10), P <0.05], ventricular tachycardia [(2.1 ± 1.3) times vs (6.3 ± 2.4) times, P <0.05] 5-HT [(51.79 ± 5.95) ng / ml vs (63.24 ± 10.21) ng / ml, P <0.05 ] And the level of oxidative stress {MDA [(2.47 ± 0.50) nmol / mg vs (4.36 ± 0.98) nmol / mg, P <0.05] and SOD [(502.22 ± 66.35) U / mg vs (392.15 ± 33.33) U / mg, P <0.05] increased expression} were significantly reduced. Conclusions RD can significantly inhibit the increase of cardiac activity and cardiac arrhythmia in MI. The mechanism may be related to inhibition of histamine, 5-HT and oxidative stress.