UCLA Cardiac Arrhythmia Center and.
UCLA Neurocardiology Research Program of Excellence, Los Angeles, California, USA.
JCI Insight. 2022 Feb 22;7(4):e155747. doi: 10.1172/jci.insight.155747.
Myocardial infarction causes pathological changes in the autonomic nervous system, which exacerbate heart failure and predispose to fatal ventricular arrhythmias and sudden death. These changes are characterized by sympathetic activation and parasympathetic dysfunction (reduced vagal tone). Reasons for the central vagal withdrawal and, specifically, whether myocardial infarction causes changes in cardiac vagal afferent neurotransmission that then affect efferent tone, remain unknown. The objective of this study was to evaluate whether myocardial infarction causes changes in vagal neuronal afferent signaling. Using in vivo neural recordings from the inferior vagal (nodose) ganglia and immunohistochemical analyses, structural and functional alterations in vagal sensory neurons were characterized in a chronic porcine infarct model and compared with normal animals. Myocardial infarction caused an increase in the number of nociceptive neurons but a paradoxical decrease in functional nociceptive signaling. No changes in mechanosensitive neurons were observed. Notably, nociceptive neurons demonstrated an increase in GABAergic expression. Given that nociceptive signaling through the vagal ganglia increases efferent vagal tone, the results of this study suggest that a decrease in functional nociception, possibly due to an increase in expression of inhibitory neurotransmitters, may contribute to vagal withdrawal after myocardial infarction.
心肌梗死导致自主神经系统发生病理变化，从而加重心力衰竭，并易引发致命性室性心律失常和猝死。这些变化的特征是交感神经激活和副交感神经功能障碍（迷走神经张力降低）。导致中枢性迷走神经传出抑制的原因，特别是心肌梗死是否会引起心脏迷走传入神经递质传递的变化，从而影响传出神经张力，目前仍不清楚。本研究旨在评估心肌梗死是否会引起迷走神经感觉神经元传入信号的变化。通过对猪慢性梗死模型和正常动物进行体内迷走神经（结状神经节）的神经记录和免疫组织化学分析，研究人员对迷走感觉神经元的结构和功能改变进行了特征描述。心肌梗死导致伤害性神经元数量增加，但功能性伤害性信号传递却出现矛盾性下降。机械敏感神经元没有变化。值得注意的是，伤害性神经元表现出 GABA 能表达增加。鉴于通过迷走神经节的伤害性信号会增加传出迷走神经张力，因此本研究结果表明，功能性伤害性传入的减少，可能是由于抑制性神经递质表达增加，可能导致心肌梗死后迷走神经传出抑制。
