The possible association between COVID-19 and postural tachycardia syndrome.
The possible association between COVID-19 and postural tachycardia syndrome.
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DOI：
10.1016/j.hrthm.2020.12.007
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发表时间：
2021-04
期刊：
影响因子：
5.5
通讯作者：
Goldstein DS
中科院分区：
文献类型：
--
作者：
Goldstein DS
坎农教授说，在紧急情况下激活交感神经系统和肾上腺有助于维持动态平衡，这是他发明的一个词。从那时起，其他神经内分泌系统也被描述为与ANS的组成部分密切相关。这些系统包括下丘脑-垂体-肾上腺皮质(HPA)系统、肾素-血管紧张素醛固酮系统(RAS)和精氨酸加压素系统。在各种应激源中，血浆肾上腺素(EPI)水平的反应与促肾上腺皮质激素(HPA轴的前垂体激素)的反应比去甲肾上腺素(NE，交感去甲肾上腺素系统(SNS)的神经递质)的反应更密切。这些发现支持交感肾上腺素能系统(SAS)和HPA轴之间的密切联系。SNS和SA反过来又与RAS紧密相连。肾小球旁细胞b1受体占位可释放肾素，肾上腺髓质嗜铬细胞具有血管紧张素受体，当被占据时可刺激肾上腺皮质激素的分泌，中枢神经肾素-血管紧张素系统参与交感神经流出的调节。血管紧张素转换酶2将血管紧张素II(AII)转化为血管紧张素1-7，而血管紧张素1-7与AII的作用相反。SARS-CoV-2通过与血管紧张素转换酶2型结合进入细胞。除了作为升压素和身体主要的保水激素外，在大脑中，血管加压素增强了对交感神经流出的压力反射抑制。EAS的第二个方面是神经免疫。众所周知，皮质醇是HPA轴的主要抗炎化合物。细胞因子白介素6激活HPA Axis2并刺激醛固酮的产生，证明了EAS的免疫和神经内分泌方面之间的联系。胆碱能抗炎途径包括细胞因子诱导的迷走神经传入交通的增加和迷走神经传出抑制炎症性细胞因子的释放。3迷走神经刺激抑制细胞因子肿瘤坏死因子a的产生，可能是通过乙酰胆碱和去甲肾上腺素这两种主要神经递质实现的。没有简单的概念来解释儿茶酚胺能对免疫的影响。尽管在各种压力情况下，EPI水平的升高与白细胞介素6的升高有关，但这种关系的基础尚不清楚。免疫细胞合成和释放儿茶酚胺，4但其功能意义尚不清楚。
Cannon taught that activation of the sympathetic nervous system and adrenal gland in emergencies helps maintain homeostasis, a word he invented. Since then, other neuroendocrine systems have been described that are closely linked to components of the ANS. These include the hypothalamic-pituitary-adrenocortical (HPA) system, the renin-angiotensinaldosterone system (RAS), and the arginine vasopressin system. Across a variety of stressors, responses of plasma epinephrine (EPI) levels are more closely tied to those of adrenocorticotropin (the anterior pituitary hormone of the HPA axis) than of norepinephrine (NE, the neurotransmitter of the sympathetic noradrenergic system (SNS)). These findings support a close association between the sympathetic adrenergic system (SAS) and the HPA axis. The SNS and SAS in turn are closely connected to the RAS. Occupation of b1 adrenoceptors in renal juxtaglomerular cells releases renin, adrenomedullary chromaffin cells possess angiotensin receptors that when occupied evoke EPI secretion, and there is a central neural renin-angiotensin system that participates in the regulation of sympathetic outflow. Angiotensinconverting enzyme type 2 converts angiotensin II (AII) to angiotensin 1–7, which opposes the effects of AII. SARS-CoV-2 enters cells via binding to angiotensin-converting enzyme type 2. In addition to being a pressor and the body’s main water-retaining hormone, in the brain vasopressin augments baroreflexive restraint of sympathetic outflows. A second aspect of the EAS is neuroimmunity. Cortisol is well known to be the major anti-inflammatory compound of the HPA axis. The cytokine interleukin 6 activates the HPA axis2 and stimulates the production of aldosterone, demonstrating links between the immunological and neuroendocrine facets of the EAS. A cholinergic anti-inflammatory pathway involves cytokine-induced increases in vagal afferent traffic and vagal efferent inhibitory effects on inflammasomal cytokine release. 3 Vagal stimulation inhibits the production of the cytokine tumor necrosis factor a, probably via the 2 main neurotransmitters of the ANS, acetylcholine and NE. No simple concept explains catecholaminergic influences on immunity. Although across a variety of stressful situations increases in EPI levels are associated with elevations of interleukin 6, bases for this relationship are poorly understood. Immune cells synthesize and release catecholamines, 4 but the functional significance is unknown.
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