The extended autonomic system, dyshomeostasis, and COVID-19

David S Goldstein, David S Goldstein

Abstract

The pandemic viral illness COVID-19 is especially life-threatening in the elderly and in those with any of a variety of chronic medical conditions. This essay explores the possibility that the heightened risk may involve activation of the "extended autonomic system" (EAS). Traditionally, the autonomic nervous system has been viewed as consisting of the sympathetic nervous system, the parasympathetic nervous system, and the enteric nervous system. Over the past century, however, neuroendocrine and neuroimmune systems have come to the fore, justifying expansion of the meaning of "autonomic." Additional facets include the sympathetic adrenergic system, for which adrenaline is the key effector; the hypothalamic-pituitary-adrenocortical axis; arginine vasopressin (synonymous with anti-diuretic hormone); the renin-angiotensin-aldosterone system, with angiotensin II and aldosterone the main effectors; and cholinergic anti-inflammatory and sympathetic inflammasomal pathways. A hierarchical brain network-the "central autonomic network"-regulates these systems; embedded within it are components of the Chrousos/Gold "stress system." Acute, coordinated alterations in homeostatic settings (allostasis) can be crucial for surviving stressors such as traumatic hemorrhage, asphyxiation, and sepsis, which throughout human evolution have threatened homeostasis; however, intense or long-term EAS activation may cause harm. While required for appropriate responses in emergencies, EAS activation in the setting of chronically decreased homeostatic efficiencies (dyshomeostasis) may reduce thresholds for induction of destabilizing, lethal vicious cycles. Testable hypotheses derived from these concepts are that biomarkers of EAS activation correlate with clinical and pathophysiologic data and predict outcome in COVID-19 and that treatments targeting specific abnormalities identified in individual patients may be beneficial.

Keywords: Adrenaline; Autonomic; COVID-19; Catecholamines; Dyshomeostasis; Homeostasis; Stress; Sympathetic.

Figures

Fig. 1
Fig. 1
From homeostasis to allostasis. In allostasis there is a shift in input-output curves for oppositely acting effectors (yellow and white), resulting in regulation of the monitored variable (in this case body temperature) at a different level. The acceptable bounds are the vertical dashed lines. A low-grade fever associated with a flu-like illness is an example of an allostatic state
Fig. 2
Fig. 2
Central stress systems. The concept diagram on the left (reproduced with permission of the American College of Physicians) shows the Chrousos and Gold model of “the central stress system.” The concept diagram on the right relates the central stress system to the central autonomic network. CING cingulate cortex, AMY amygdala, Hippo hippocampus, PVN paraventricular nucleus of the hypothalamus, HACER hypothalamic area controlling emotional responses, AVP arginine vasopressin (same as anti), CRH corticotropin-releasing hormone, VTA ventral tegmental area, PAG periaqueductal gray, LC locus ceruleus, A5 A5 noradrenergic cell group, RTN retrotrapezoid nucleus, RVLM rostral ventrolateral medulla, AP area postrema, PBN parabrachial nucleus, Pre-Botz. pre-Botzinger complex, NTS nucleus of the solitary tract, CVLM caudal ventrolateral medulla, NA nucleus ambiguus, DMNX dorsal motor nucleus of the vagus nerve, RPG respiratory pattern generator, ACTH adrenocorticotrophic hormone (corticotropin), ANS autonomic nervous system, SNS sympathetic noradrenergic system (norepinephrine), SAS sympathetic adrenergic system (adrenaline), PNS parasympathetic nervous system (acetylcholine)
Fig. 3
Fig. 3
From EAS system activation to dyshomeostasis to death. Five effector components of the EAS are on the left. Intervening variables are in the center. Factors contributing the critical illness or death are on the right. The red bar under PNS indicates PNS inhibition. AI angiotensin I, ACE angiotensin-converting enzyme, AII angiotensin II, Aldo aldosterone, ATN acute tubular necrosis, IL-6 interleukein 6, Myo. myocardial, Cor. coronary, TNFa tumor necrosis factor alpha

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