Preprint Hypothesis Version 1 Preserved in Portico This version is not peer-reviewed

Interference of SARS-CoV-2 with the Homeostasis of Ventilation and Perfusion in the Lung

Version 1 : Received: 10 May 2020 / Approved: 10 May 2020 / Online: 10 May 2020 (17:22:59 CEST)

How to cite: Arias, C.F.; Acosta, F.J.; Bertocchini, F.; Fernández-Arias, C. Interference of SARS-CoV-2 with the Homeostasis of Ventilation and Perfusion in the Lung. Preprints 2020, 2020050177. https://doi.org/10.20944/preprints202005.0177.v1 Arias, C.F.; Acosta, F.J.; Bertocchini, F.; Fernández-Arias, C. Interference of SARS-CoV-2 with the Homeostasis of Ventilation and Perfusion in the Lung. Preprints 2020, 2020050177. https://doi.org/10.20944/preprints202005.0177.v1

Abstract

A growing number of studies suggest that SARS-CoV-2 could interfere with homeostatic mechanisms in the lung but the implications of this possible interference have not been fully explored in the literature. In this work, we examine the consequences that can be drawn from this hypothesis according to currently available knowledge. We suggest that one such consequence is the potential disruption of normal ventilation and perfusion of lung regions that may be distant from the infection sites. Loss of ventilation might result in local alveolar hypoxia and contribute to hypoxemia, which in turn could trigger homeostatic responses that enhance blood oxygenation by redistributing pulmonary blood circulation. Sudden changes in perfusion might then lead to the development of hydrostatic edema and eventually to vascular remodeling and inflammation. Therefore, the immune response might not be the only source of the substantial inflammation observed in lung tissues of patients with severe COVID-19, as is often assumed in the literature. The balance between the homeostatic and the immune reaction in each patient could account for the observed heterogeneity of the clinical manifestations of COVID-19.

Keywords

SARS-CoV-2; COVID-19; homeostasis; hypoxic pulmonary vasoconstriction; renin-angiotensin system; hydrostatic edema; permeability edema

Subject

Biology and Life Sciences, Anatomy and Physiology

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