摘要
目的探讨交感神经活性与神经重构在犬心肌梗死后新发心房颤动（房颤）中的作用。方法将12只犬采用随机数字表法分为对照组（6只）和模型组（6只）。对照组只开胸，不结扎血管；模型组采用结扎冠状动脉左回旋支和右冠状动脉心房支的方法构建心肌梗死后新发房颤模型。记录基础状态、缺血30min、2h、4h房颤诱发率、交感神经放电幅度及频率，高效液相色谱法测定心肌和肾脏的去甲。肾上腺素（NE）、肾上腺素（E）浓度。结果①模型组术后30min（50．8％对6．7％）、2h（95．8％对13．3％）、4h（91．7％对26．7％）的房颤诱发率显著高于对照组和基础状态（P〈0．05）；②与对照组相比，模型组术后5、30min的交感神经放电频率明显增多（5min：515对380，P=0．002；30min：495对383，P=0．009）、幅度明显增大[交感神经放电均方根Apeak值：（903．28±51．69）μV对（589．56±48．28）μV，P〈0．05；（783．52±34．55）μV对（559．23±32．83）μV，P〈0．05]；③心肌和肾脏中的NE、E浓度显著高于对照组（P〈0．05）。结论心肌梗死后存在交感神经过度激活，心肌梗死后房颤的发生与交感神经活性密切相关。
Objective We aimed to determine the contribution of sympathetic neural remodeling to the occurrence of atrial fibrillation（AF） after acute myocardial infarction（AMI）. And to observe the influence of myocardial infarction on the AF induction rate and sympathetic neural remodeling. Methods We randomly divided 12 dogs into 2 groups, control group （ n = 6 ） model group （ n = 6 ） using random number table. We applied open heart surgery without ligating the vessels in control group. And in model group we ligated the left circumflex artery （LCX） and right atrial branch of right coronary artery to induce AF after AMI. AF induction rate during baseline, 30 minutes,2 hours ,4 hours after ischemia and the amplitude and frequency of sympathetic nerve discharge were recorded during baseline,5 minutes, 30 minutes, 2 hours after ischemia. The density of norepinephrine,and epinephrine in myocardium and kidney were determined by high performance liguid chro- matography （HPLC）. Results The AF induction rate 30 minutes（50. 8% vs. 6. 7%） ,2 hours（95.8% vs. 13.3% ） ,and 4 hours（91.7% vs. 26.7% ） after ischemia in model group was significantly higher that incontrol group and baseline（P〈0. 05）, the inciduction rate before ligation. The amplitude and frequency of sympathetic nerve discharge 5 minutes, and 30 minutes after ischemia were larger than that in control group [the root mean square peak value of sympathetic neural discharging： （903.28＋51.69） /zV vs. （589.56＋ 48.28） IxV,P〈0. 05;（783.52＋34. 55） txV vs. （559. 23＋32. 83） IxV,P〈0. 05; frequency：515 vs. 380,P= 0. 002 ;495 vs. 383 ,P= 0. 0091. The density of NE and E in model group was significantly higher when com- pared with control group （P〈0. 05 ）. Conclusion Excessive sympathetic nerve activation was observed after myocardial infarction. The occurrence of AF after AMI was closely related to the sympathetic neural activity.
出处
《中华心律失常学杂志》
2015年第6期440-444,共5页
Chinese Journal of Cardiac Arrhythmias
基金
国家自然科学基金（81460054）,新疆维吾尔自治区心血管病研究实验室开放课题（X,JDX0903-2013-03）,新疆医科大学第一附属医院自然科学基金重点项目（2013ZRZD01）
关键词
心肌梗死
心房颤动
交感神经活性
Myocardial infarction
Atrial fibrillation
Sympathetic neural activity
