| 张 秀,程怡慧,张心彤,王 璐,滕美玲,陆 晓.生理性缺血训练改善心肌梗死后慢性心力衰竭大鼠心功能及心室重塑的神经机制[J].中国康复医学杂志,2021,(8):915~922 |
| 生理性缺血训练改善心肌梗死后慢性心力衰竭大鼠心功能及心室重塑的神经机制 点此下载全文 |
| 张 秀 程怡慧 张心彤 王 璐 滕美玲 陆 晓 |
| 南京医科大学第一附属医院康复医学中心，江苏省南京市，210029 |
| 基金项目：国家自然科学基金面上项目（81772441）；国家自然科学基金青年科学基金项目（81902288）；苏州市临床医学专家团队引进项目（SZYJTD201725）；南京市功能重建与康复临床医学研究中心项目（2019060002） |
| DOI：10.3969/j.issn.1001-1242.2021.08.003 |
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| 摘要： |
| 摘要
目的：探讨生理性缺血训练（PIT）改善心肌梗死后慢性心衰大鼠心功能及心室重塑的神经机制。
方法：健康雄性Wistar大鼠随机分为生理性缺血训练组（PIT组）、迷走神经切断组（VN-cut组）、单纯心衰组（CHF组）及假手术组（SO组）。采用结扎左冠状动脉前降支的方法制备心肌梗死后慢性心衰模型。PIT组进行慢性心衰造模，同时进行PIT，PIT方案为双下肢缺血5min，再灌注5min，5次/天，5天/周，持续8周；VN-cut组进行慢性心衰及右侧迷走神经切断造模，同时进行PIT；CHF组进行慢性心衰造模，不进行PIT；SO组大鼠行开胸手术，6-0结扎线穿过心脏而不结扎，不进行PIT，安静笼养。训练8周后，采用小动物超声心动图检测心功能，随后取左心室肌进行以下检测：Masson染色测心肌梗死面积，RT-PCR检测Bcl-2/Bax及MMP9/TIMP-1的mRNA含量，Ellman法检测乙酰胆碱酯酶活性，Karnoysky-Roots法检测胆碱能神经密度。
结果：训练8周后，PIT组与CHF组相比，左室射血分数（LVEF）、Bcl-2/Bax及MMP9/TIMP-1的比值、乙酰胆碱酯酶活性、胆碱能神经密度改善均有显著性意义（P<0.05）。PIT组与VN-cut组相比，LVEF、心肌梗死面积、Bcl-1/Bax及MMP9/TIMP-1的比值、胆碱能神经密度改善均有显著性意义（P<0.05），CHF组与VN-cut组相比Bcl-1/Bax及MMP9/TIMP-1的比值改善有显著性意义（P<0.05）。相关性分析显示，Bcl-2/Bax的比值与乙酰胆碱酯酶活性、胆碱能神经密度之间呈直线正相关(P<0.01)，而MMP9/TIMP-1的比值与乙酰胆碱酯酶活性、胆碱能神经密度之间呈直线负相关（P<0.01）。
结论：生理性缺血训练通过提高乙酰胆碱酯酶活性及胆碱能神经密度，进而提高迷走神经活性。相关性分析表明，心肌梗死后心室重构受迷走神经活性相关因子调控，因此，有理由推测生理性缺血训练可调控迷走神经活性相关因子改善心肌梗死后慢性心衰大鼠的心功能及心室重塑。 |
| 关键词：生理性缺血训练 迷走神经 心功能 心室重塑 |
| Neural mechanism of physiological ischemic training in improving cardiac function and ventricular remodeling in chronic heart failure after myocardial infarction Download Fulltext |
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| Dept. of Rehabilitation Medicine， the First Affiliated Hospital of Nanjing Medical University， Nanjing， Jiangsu， 210029 |
| Fund Project: |
| Abstract: |
| Abstract
Objective： To investigate the neural mechanism of physiological ischemic training (PIT) in improving cardiac function and ventricular remodeling in rats with chronic heart failure induced by myocardial infarction.
Method： Healthy male Wistar rats were randomized into physiological ischemia training group (PIT group)， vagal nerve cut group (VN-cut group)， chronic heart failure group (CHF group) and sham operation group (SO group). The chronic heart failure model was prepared by ligating the anterior descending branch of left coronary artery (LAD). The PIT group received PIT training in addition to thoracotomy and LAD ligation. The PIT training protocol was consisted of 5 min of ischemia followed by 5 min of perfusion， 5 cycles a day， 5 days per week for 8 weeks. The right vagal nerve was cut off in the VN-cut group in addition to thoracotomy， LAD ligation and PIT training. The CHF group received both thoracotomy and LAD ligation. Rats in the SO group only received thoracotomy with no ligation or training. After 8 weeks of training， cardiac function was detected with echocardiography. Masson staining was used to measure size of myocardial infarction. RT-PCR was used to detect mRNA concentration of Bcl-1/Bax and MMP9/TIMP-1. Ellman method was used to detect acetylcholinesterase activity， and Karnoysky-Roots method was for cholinergic nerve density.
Result： After 8 weeks training， the left ventricular ejection fraction (LVEF)， the ratio of Bcl-2/Bax and MMP9/TIMP-1， the acetylcholinesterase activity， and the cholinergic nerve density were improved significantly in the PIT group when compared with those in the CHF group (P<0.05). Compared with the VN-cut group， the PIT group significantly improved the LVEF， the myocardial infarction area， the ratio of Bcl-2/Bax and MMP9/TIMP-1， and the cholinergic nerve density (P<0.05). Compared with the VN-cut group， the improvement in the ratio of Bcl-2/Bax and MMP9/TIMP-1 was statistically significant in the CHF group (P<0.05). Correlation analysis showed that the ratio of Bcl-2/Bax was positively correlated with the acetylcholinesterase activity and cholinergic nerve density (P<0.01)， while the ratio of MMP9/TIMP-1 was negatively correlated with the acetylcholinesterase activity and cholinergic nerve density (P<0.01).
Conclusion： Physiological ischemia training was able to upregulate vagal nerve activity by increasing the acetylcholinesterase activity and cholinergic nerve density. Correlation analysis showed that ventricular remodeling was regulated by vagal activity， thus concluding that PIT can preliminarily improve cardiac function and ventricular remodeling through the upregulation of vagal activity in rats with chronic heart failure after myocardial infarction. |
| Keywords:physiological ischemic training vagal nerve cardiac function ventricular remodeling |
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