Chen R P, Thompson G W, Armour J A
Department of Pediatrics, Faculty of Medicine, Daihousie University, Halifax, Nova Scotia, Canada B3H 4H7.
Auton Neurosci. 2001 Feb 20;87(1):1-8. doi: 10.1016/S1566-0702(00)00213-7.
We sought to determine the capacity of ventricular sensory nerve endings (neurites) associated with neonatal nodose ganglion afferent neurons to transduce mechanical and chemical stimuli in situ. Spontaneous activity generated by 17 nodose ganglion cardiac afferent neurons was identified in 8 anesthetized neonatal pigs (10-21 days old) using extracellular recording recording techniques. The activity generated by afferent neurons was studied when their ventricular sensory neurites were exposed to local mechanical or chemical stimuli, following systemic administration of specific chemicals or during brief periods of apnea. Gentle mechanical distortion of their ventricular sensory fields enhanced the activity generated by 6 spontaneously active afferent neurons, while suppressing the activity generated by another 3 neurons. Afferent neuronal activity was either enhanced or suppressed when the following chemicals were applied to identified ventricular epicardial sensory fields: the sodium channel modifier veratridine (92% of tested neurons); the P1-purinoceptor agonist adenosine (92%); the neuropeptides angiotensin II (100%), bradykinin (90%) and substance P (90%); and the nitric oxide donor S-nitroso-N-acetylpenicillamine (100%). Epicardial application of isoproternol or nicotine induced modest neuronal responses. Cardiac afferent neurons were also affected when these chemicals were administered systemically. Apnea of 60-100 s duration modified (enhanced, n = 2; suppressed, n = 5) the activity generated by most identified afferent neurons. The estimated average conduction velocity of afferent axons associated with these neurons was 1.0 +/- 0.2 m/s. It is concluded that neonatal nodose ganglion cardiac afferent neurons respond to many of the chemicals known to modify adult cardiac afferent neurons. That cardiac afferent neurons are capable of sensing the mechanical and chemical milieu of the neonatal heart should be taken into account when considering altered neonatal cardiovascular status such as occurs during apnea.
我们试图确定与新生结节神经节传入神经元相关的心室感觉神经末梢（神经突）在原位转导机械和化学刺激的能力。使用细胞外记录技术，在8只麻醉的新生猪（10 - 21日龄）中识别出17个结节神经节心脏传入神经元产生的自发活动。在其心室感觉神经突暴露于局部机械或化学刺激时、在全身给予特定化学物质后或在短暂呼吸暂停期间，研究传入神经元产生的活动。对其心室感觉野进行轻柔的机械扭曲增强了6个自发活动传入神经元产生的活动，同时抑制了另外3个神经元产生的活动。当将以下化学物质应用于已识别的心室心外膜感觉野时，传入神经元活动增强或受到抑制：钠通道调节剂藜芦碱（92%的受试神经元）；P1嘌呤受体激动剂腺苷（92%）；神经肽血管紧张素II（100%）、缓激肽（90%）和P物质（90%）；以及一氧化氮供体S - 亚硝基 - N - 乙酰青霉胺（100%）。心外膜应用异丙肾上腺素或尼古丁引起适度的神经元反应。当全身给予这些化学物质时，心脏传入神经元也受到影响。持续60 - 100秒的呼吸暂停改变了（增强，n = 2；抑制，n = 5）大多数已识别传入神经元产生的活动。与这些神经元相关的传入轴突的估计平均传导速度为1.0 +/- ）0.2米/秒。结论是，新生结节神经节心脏传入神经元对许多已知可改变成年心脏传入神经元的化学物质有反应。在考虑新生儿心血管状态改变（如呼吸暂停期间发生的情况）时，应考虑到心脏传入神经元能够感知新生儿心脏的机械和化学环境。
