Dynamic remodeling of the guinea pig intrinsic cardiac plexus induced by chronic myocardial infarction.
Dynamic remodeling of the guinea pig intrinsic cardiac plexus induced by chronic myocardial infarction.
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DOI：
10.1016/j.autneu.2013.10.008
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发表时间：
2014-04
影响因子：
2.7
通讯作者：
Southerland, E. Marie
中科院分区：
文献类型：
--
作者：
Hardwick, Jean C.;Ryan, Shannon E.;Beaumont, Eric;Ardell, Jeffrey L.;Southerland, E. Marie
关键词：
心肌梗死（MI）与心脏和神经体液控制系统的重塑有关。本研究的目的是确定心肌梗死后内在心脏（IC）神经元兴奋性、突触功效和神经化学调节的时间依赖性变化。通过结扎豚鼠心脏背侧表面上的冠状动脉和相关静脉来产生MI。动物恢复4、7、14或50天。在整个心脏神经丛中获得细胞内电压记录，以确定IC神经元的被动和主动神经元特性。免疫组化分析表明，IC神经元的神经元型一氧化氮合酶的免疫反应的百分比立即和持续增加。个别神经元的性能检查表明，后超极化电位的幅度和恢复的时间过程中，在MI后7天显着降低。MI后50天，这些参数恢复至对照值。通过轴突输入的刺激确定的突触功效仅在MI后7天增强。在没有激动剂的挑战神经元兴奋性是不变的MI。去甲肾上腺素增加IC对细胞内电流注入的兴奋性，这是MI后增强的反应。心肌梗死后，血管紧张素II增强去甲肾上腺素和氨甲酰胆碱诱导的兴奋性，在对照组中明显。这项研究表明，MI诱导持久性和短暂性的变化，IC神经元功能损伤后立即。IC神经元网络的改变在初始损伤后持续数周，可能导致自主信号传导和心脏控制的改变。
Myocardial infarction (MI) is associated with remodeling of the heart and neurohumoral control systems. The objective of this study was to define time-dependent changes in intrinsic cardiac (IC) neuronal excitability, synaptic efficacy, and neurochemical modulation following MI. MI was produced in guinea pigs by ligation of the coronary artery and associated vein on the dorsal surface of the heart. Animals were recovered for 4, 7, 14, or 50 days. Intracellular voltage recordings were obtained in whole mounts of the cardiac neuronal plexus to determine passive and active neuronal properties of IC neurons. Immunohistochemical analysis demonstrated an immediate and persistent increase in the percentage of IC neurons immunoreactive for neuronal nitric oxide synthase. Examination of individual neuronal properties demonstrated that afterhyperpolarizing potentials were significantly decreased in both amplitude and time course of recovery at 7 days post-MI. These parameters returned to control values by 50 days post-MI. Synaptic efficacy, as determined by the stimulation of axonal inputs, was enhanced at 7 days post-MI only. Neuronal excitability in absence of agonist challenge was unchanged following MI. Norepinephrine increased IC excitability to intracellular current injections, a response that was augmented post-MI. Angiotensin II potentiation of norepinephrine and bethanechol-induced excitability, evident in controls, was abolished post-MI. This study demonstrates that MI induces both persistent and transient changes in IC neuronal functions immediately following injury. Alterations in the IC neuronal network, which persist for weeks after the initial insult, may lead to alterations in autonomic signaling and cardiac control.
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DOI：
10.1152/ajpregu.00223.2012
发表时间：
2012-11-01
影响因子：
2.8
作者：
Hardwick, Jean C.;Southerland, E. Marie;Ardell, Jeffrey L.
通讯作者：
Ardell, Jeffrey L.
DOI：
10.1016/0165-1838(94)00182-j
发表时间：
1995-06-25
期刊：
JOURNAL OF THE AUTONOMIC NERVOUS SYSTEM
影响因子：
--
作者：
HARDWICK, JC;MAWE, GM;PARSONS, RL
通讯作者：
PARSONS, RL
DOI：
10.1152/ajpregu.00123.2003
发表时间：
2003-09-01
影响因子：
2.8
作者：
Jelson, GS;DeMasi, GM;Hardwick, JC
通讯作者：
Hardwick, JC
DOI：
10.1152/ajpheart.00498.2007
发表时间：
2009-07-01
影响因子：
4.8
作者：
Gonzalez, German E.;Seropian, Ignacio M.;Morales, Celina
通讯作者：
Morales, Celina
影响因子：
2.5
作者：
Ewert, T. Jarred;Gritman, Kurt R.;Habecker, Beth A.
通讯作者：
Habecker, Beth A.