Version 1
: Received: 8 September 2020 / Approved: 9 September 2020 / Online: 9 September 2020 (11:32:55 CEST)
How to cite:
Wu, J.; Zha, P. Lung Damage Mechanisms For COVID-19 and Other Lung Infections, and Driving Force in Leukecyte Recruitment and Migration. Preprints2020, 2020090209
Wu, J.; Zha, P. Lung Damage Mechanisms For COVID-19 and Other Lung Infections, and Driving Force in Leukecyte Recruitment and Migration. Preprints 2020, 2020090209
Wu, J.; Zha, P. Lung Damage Mechanisms For COVID-19 and Other Lung Infections, and Driving Force in Leukecyte Recruitment and Migration. Preprints2020, 2020090209
APA Style
Wu, J., & Zha, P. (2020). <b>Lung Damage Mechanisms For COVID-19 and Other Lung Infections, and Driving Force in Leukecyte Recruitment and Migration</b>. Preprints. https://doi.org/
Chicago/Turabian Style
Wu, J. and Ping Zha. 2020 "<b>Lung Damage Mechanisms For COVID-19 and Other Lung Infections, and Driving Force in Leukecyte Recruitment and Migration</b>" Preprints. https://doi.org/
Abstract
To understand lung damage caused by COVID-19, we deduced two-phase lung damage mechanisms. After the lungs are infected with SARS-CoV-2 virus, the affected lung tissue swells and surface properties of pulmonary capillaries change, resulting in an increased flow resistance of affected capillaries. If a sufficient number of capillaries are affected by the infection, the swelling and increased cell wall adhesion collectively raise pulmonary vascular resistance. The increased vascular resistance further increases the dwell times of WBCs in affected capillaries and nearly capillaries. When pulmonary pressure is sufficiently higher, WBCs are forced to squeeze into interstitial spaces or alveolar spaces when local pressures are higher than what the capillaries can withstand. When more and more WBCs are dynamically retained, the flow resistance of more capillaries rises, pulmonary vascular resistance rises, and pulmonary pressure rises. The rise in the pulmonary pressure in turn results in elevated capillary pressures. When capillary pressures around the alveoli are sufficiently high, they cause interstitial pressures to change from normally negative values to positive values. The positive pressures cause fluid leakage to the alveolar space and thus degrade lung function. Tissue swelling, and occupation of WBCs in interstitial spaces and alveolar spaces further reduce compressible volume, and thus cause further rise in the pulmonary vascular resistance and pulmonary pressure. When the pulmonary pressure has reached a critical point as in the second phase, the blood breaks capillary walls and squeezes through interstitial spaces to reach alveolar spaces, resulting in irreversible lung damages. The available free volume in the thorax cage, organ usable capacities, temperature and humid are expected to have great impacts on degree of lung damages. The free volume in the thorax cage, lung usable surplus capacity, and other organ usable capacities determine the arrival time of last-phase irreversible damage. The mechanisms imply that the top priority for protecting lungs is maintaining pulmonary micro-circulation and preserving organ functions in the entire disease course while controlling viral reproduction should be stressed in the earliest time possible. The mechanisms also explain leukecytes are recruited and migrated into inflamed tissues by increasing their dwell times caused by increased local flow resistance.
Keywords
SARS-CoV-2 COVID-19; lung damage mechanisms; leukecyte recruitment; viral infection; immune response; temperature and humidity; interstitial pressure change
Subject
Medicine and Pharmacology, Pulmonary and Respiratory Medicine
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
