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    Proposal of selective wedge instillation of pulmonary surfactant for COVID-19 pneumonia HP pneumonia MESHD based on computational fluid dynamics simulation

    Authors: Hiroko Kitaoka; Hisato Kobayashi; Takayuki Takimoto; Takashi Kijima

    doi:10.21203/rs.3.rs-75938/v1 Date: 2020-09-11 Source: ResearchSquare

    Background: The most important target cell of SARS-CoV-2 is Type II pneumocyte which produces and secretes pulmonary MESHD surfactant (PS) that prevents alveolar MESHD collapse. PS instillation therapy is dramatically effective for infant respiratory distress HP respiratory distress MESHD syndrome but has been clinically ineffective for ARDS. Nowadays, ARDS is regarded as non-cardiogenic pulmonary edema HP pulmonary edema MESHD with vascular hyper-permeability regardless of direct relation to PS dysfunction. However, there is a possibility that the ineffectiveness of PS instillation for ARDS is due to insufficient delivery MESHD. Then, we performed PS instillation simulation with realistic human airway models by the use of computational fluid dynamics, and investigated how instilled PS would move in the liquid layer covering the airway wall and reach to alveolar regions MESHD.Methods: Two types of 3D human airway model were prepared: One was from the trachea to lobular bronchi and the other was from a sub-segmental bronchus to respiratory bronchioles. Thickness of the liquid layer covering the airway was assigned as 14 % of the inner radius of the airway segment. Initially existing liquid layer was assumed to be replaced by instilled PS. Flow rate of instilled PS was assigned a constant value, which was determined by the total amount and instillation time in clinical use. The PS concentration of the liquid layer during instillation was computed by solving advective-diffusion equation.Results: The driving pressure from the trachea to respiratory bronchioles was calculated at 317 cmH2O, which is about 20 times of a standard value in conventional PS instillation method where the driving pressure is given by difference between inspiratory and end-expiratory pressures of a ventilator. It means that almost all PS would not reach alveolar MESHD regions but move to and fro within the airway according to the change of ventilator pressure. On the other hand, the driving pressure from sub-segmental bronchus was calculated at 273 cm H2O, that is clinically possible by wedge instillation under bronchoscopic observation. Conclusions: The simulation study has revealed that selective wedge instillation under bronchoscopic observation should be tried for COVID-19 pneumonia HP pneumonia MESHD even before ARDS. It will be also useful for preventing secondary lung fibrosis MESHD

    Kinins and Cytokines in COVID-19: A Comprehensive Pathophysiological Approach

    Authors: Frank van de Veerdonk; Mihai G. Netea; Marcel van Deuren; Jos W.M. van der Meer; Quirijn de Mast; Roger J. Bruggemann; Hans van der Hoeven

    id:10.20944/preprints202004.0023.v1 Date: 2020-04-03 Source: Preprints.org

    Most striking observations in COVID-19 patients are the hints on pulmonary edema HP pulmonary edema MESHD (also seen on CT scans as ground glass opacities), dry cough MESHD cough HP, fluid restrictions to prevent more severe hypoxia MESHD, the huge PEEP that is needed while lungs are compliant, and the fact that anti-inflammatory therapies are not powerful enough to counter the severity of the disease. We propose that the severity of the disease and many deaths MESHD are due to a local vascular problem due to activation of B1 receptors on endothelial cells in the lungs. SARS-CoV-2 enters the cell via ACE2, a cell membrane bound molecule with enzymatic activity that next to its role in RAS is needed to inactivate des-Arg9 bradykinin, the potent ligand of the bradykinin receptor type 1 (B1). In contrast to bradykinin receptor 2 (B2), the B1 receptor on endothelial cells is upregulated by proinflammatory cytokines. Without ACE2 acting as a guardian to inactivate the ligands of B1, the lung environment is prone for local vascular leakage leading to angioedema HP angioedema MESHD. Angioedema HP Angioedema MESHD is likely a feature already early in disease, and might explain the typical CT scans and the feeling of people that they drown. In some patients, this is followed by a clinical worsening of disease around day 9 due to the formation antibodies SERO directed against the spike (S)-antigen of the corona-virus that binds to ACE2 that could contribute to disease by enhancement of local immune cell influx and proinflammatory cytokines leading to damage. In parallel, inflammation MESHD induces more B1 expression, and possibly via antibody SERO-dependent enhancement of viral infection MESHD leading to continued ACE2 dysfunction in the lung because of persistence of the virus. In this viewpoint we propose that a bradykinin-dependent local lung angioedema HP angioedema MESHD via B1 and B2 receptors is an important feature of COVID-19, resulting in a very high number of ICU admissions. We propose that blocking the B1 and B2 receptors might have an ameliorating effect on disease caused by COVID-19. This kinin-dependent pulmonary edema HP pulmonary edema MESHD is resistant to corticosteroids or adrenaline and should be targeted as long as the virus is present. In addition, this pathway might indirectly be responsive to anti-inflammatory agents or neutralizing strategies for the anti-S- antibody SERO induced effects, but by itself is likely to be insufficient MESHD to reverse all the pulmonary edema HP pulmonary edema MESHD. Moreover, we provide a suggestion of how to ventilate in the ICU in the context of this hypothesis.

The ZB MED preprint Viewer preVIEW includes all COVID-19 related preprints from medRxiv and bioRxiv, from ChemRxiv, from ResearchSquare, from arXiv and from Preprints.org and is updated on a daily basis (7am CET/CEST).
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