Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand.
Cardiac Electrophysiology Unit, Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand.
Int J Mol Sci. 2018 Aug 21;19(9):2466. doi: 10.3390/ijms19092466.
Acute myocardial infarction (AMI) is the most common cause of acute myocardial injury and its most clinically significant form. The most effective treatment for AMI is to restore an adequate coronary blood flow to the ischemic myocardium as quickly as possible. However, reperfusion of an ischemic region can induce cardiomyocyte death, a phenomenon termed "myocardial ischemia/reperfusion (I/R) injury". Disruption of cardiac parasympathetic (vagal) activity is a common hallmark of a variety of cardiovascular diseases including AMI. Experimental studies have shown that increased vagal activity exerts cardioprotective effects against myocardial I/R injury. In addition, acetylcholine (ACh), the principle cardiac vagal neurotransmitter, has been shown to replicate the cardioprotective effects of cardiac ischemic conditioning. Moreover, studies have shown that cardiomyocytes can synthesize and secrete ACh, which gives further evidence concerning the importance of the non-neuronal cholinergic signaling cascades. This suggests that the activation of ACh receptors is involved in cardioprotection against myocardial I/R injury. There are two types of ACh receptors (AChRs), namely muscarinic and nicotinic receptors (mAChRs and nAChRs, respectively). However, the effects of AChRs activation in cardioprotection during myocardial I/R are still not fully understood. In this review, we summarize the evidence suggesting the association between AChRs activation with both electrical and pharmacological interventions and the cardioprotection during myocardial I/R, as well as outline potential mechanisms underlying these cardioprotective effects.
急性心肌梗死（AMI）是急性心肌损伤最常见的原因，也是其最具临床意义的形式。AMI 最有效的治疗方法是尽快恢复缺血心肌的足够冠状动脉血流。然而，缺血区域的再灌注会诱导心肌细胞死亡，这种现象称为“心肌缺血/再灌注（I/R）损伤”。心脏副交感神经（迷走神经）活动的中断是包括 AMI 在内的多种心血管疾病的共同特征。实验研究表明，增加迷走神经活动对心肌 I/R 损伤具有心脏保护作用。此外，乙酰胆碱（ACh），心脏迷走神经递质的主要成分，已被证明可以复制心脏缺血预适应的心脏保护作用。此外，研究表明心肌细胞可以合成和分泌 ACh，这进一步证明了非神经胆碱能信号级联的重要性。这表明 ACh 受体的激活参与了心肌 I/R 损伤的心脏保护。有两种类型的 ACh 受体（AChRs），即毒蕈碱和烟碱受体（mAChRs 和 nAChRs）。然而，AChRs 激活在心肌 I/R 期间的心脏保护作用仍不完全清楚。在这篇综述中，我们总结了证据，表明 AChRs 激活与电和药理学干预以及心肌 I/R 期间的心脏保护之间存在关联，并概述了这些心脏保护作用的潜在机制。
