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首页> 外文期刊>American Journal of Physiology >Neurotransmission to parasympathetic cardiac vagal neurons in the brain stem is altered with left ventricular hypertrophy-induced heart failure
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Neurotransmission to parasympathetic cardiac vagal neurons in the brain stem is altered with left ventricular hypertrophy-induced heart failure

机译：脑干中副交感神经心脏迷离神经元的神经递质被左心室肥大诱导的心力衰竭改变

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Hypertension, cardiac hypertrophy, and heart failure (HF) are widespread and debilitating cardiovascular diseases that affect nearly 23 million people worldwide. A distinctive hallmark of these cardiovascular diseases is autonomic imbalance, with increased sympathetic activity and decreased parasympathetic vagal tone. Recent device-based approaches, such as implantable vagal stimulators that stimulate a multitude of visceral sensory and motor fibers in the vagus nerve, are being evaluated as new therapeutic approaches for these and other diseases. However, little is known about how parasympathetic activity to the heart is altered with these diseases, and this lack of knowledge is an obstacle in the goal of devising selective interventions that can target and selectively restore parasympathetic activity to the heart. To identify the changes that occur within the brain stem to diminish the parasympathetic cardiac activity, left ventricular hypertrophy was elicited in rats by aortic pressure overload using a transaortic constriction approach. Cardiac vagal neurons (CVNs) in the brain stem that generate parasympathetic activity to the heart were identified with a retrograde tracer and studied using patch-clamp electrophysiological recordings in vitro. Animals with left cardiac hypertrophy had diminished excitation of CVNs, which was mediated both by an augmented frequency of spontaneous inhibitory GABAergic neurotransmission (with no alteration of inhibitory glycinergic activity) as well as a diminished amplitude and frequency of excitatory neurotransmission to CVNs. Opportunities to alter these network pathways and neu-rotransmitter receptors provide future targets of intervention in the goal to restore parasympathetic activity and autonomic balance to the heart in cardiac hypertrophy and other cardiovascular diseases.
机译：高血压，心脏肥大和心力衰竭（HF）是普遍的和衰弱的心血管疾病，影响全世界近2300万人。这些心血管疾病的独特标志是自主失衡，具有较高的交感神经活性和减少的副交感神经迷走。最近的基于装置的方法，例如刺激迷走神经中众多内脏感官和电动纤维的可植入迷住刺激器，被评为这些和其他疾病的新治疗方法。然而，关于如何用这些疾病改变心脏对比度的副交感神经活性甚少，并且这种缺乏知识是目的是设计能够靶向和选择性地恢复心脏副交感神活性的选择性干预措施的障碍。为了确定脑干内发生的变化，以减少副交感神经活性，通过使用横向收缩方法通过主动脉压力过载在大鼠中引发左心室肥大。用逆行示踪器鉴定生成副交感神经活性的脑干中的心脏迷住神经元（CVN），并使用逆行示踪器鉴定了逆行示踪性，并在体外使用贴片电生理记录进行研究。具有左心肺肥大的动物减少了CVN的激发，其通过增强的自发抑制性胃肠杆菌（没有抑制甘油池能活性）的增强频率介导，以及兴奋性神经递质的减少幅度和频率。改变这些网络途径和Neu-Rotransmitter受体的机会提供了未来的干预目标，以恢复副交感神经活动和对心脏肥大和其他心血管疾病的心脏的自主平衡。

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