Pulmonary Edema in COVID19A Neural Hypothesis

• Published in: ACS Chemical Neuroscience Vol. 11; no. 14; pp. 2048 - 2050
• Main Authors: U.R, Anoop, Verma, Kavita
• Format: Journal Article Web Resource
• Language: English
• Published: United States American Chemical Society 15.07.2020
• Subjects: Betacoronavirus; Capillary Permeability - physiology; Coronavirus Infections - immunology; Coronavirus Infections - physiopathology; COVID-19; Cytokine Release Syndrome - immunology; Cytokine Release Syndrome - physiopathology; Facial Nerve; Glossopharyngeal Nerve; Humans; Hypotension - physiopathology; Inflammation; Lung - blood supply; Lung - immunology; Microvessels - immunology; Microvessels - physiopathology; Pandemics; Parasympathetic Nervous System - physiopathology; Pneumonia, Viral - immunology; Pneumonia, Viral - physiopathology; Pulmonary Edema - immunology; Pulmonary Edema - physiopathology; SARS-CoV-2; Solitary Nucleus - immunology; Solitary Nucleus - physiopathology; Thrombosis - physiopathology; Vagus Nerve; Vasoconstriction; Viewpoint; COVID-19; Catecholamine storm; Nucleus tractus solitarius; Brain trigger zones; Neurogenic pulmonary edema; Microvascular clotting
• DOI: 10.1021/acschemneuro.0c00370
• ISSN: 1948-7193

In COVID-19, lung manifestations present as a slowly evolving pneumonia with insidious early onset interstitial pulmonary edema that undergoes acute exacerbation in the late stages and microvascular thrombosis. Currently, these manifestations are considered to be only consequences of pulmonary SARS-CoV-2 virus infection. We are proposing a new hypothesis that neurogenic insult may also play a major role in the pathogenesis of these manifestations. SARS-CoV-2 mediated inflammation of the nucleus tractus solitarius (NTS) may play a role in the acute exacerbation of pulmonary edema and microvascular clotting in COVID-19 patients.