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Comment
. 2020 Jun;46(6):1105-1108.
doi: 10.1007/s00134-020-06059-6. Epub 2020 Apr 28.

Facing COVID-19 in the ICU: vascular dysfunction, thrombosis, and dysregulated inflammation

Daniel E Leisman  1 , Clifford S Deutschman  2 , Matthieu Legrand  3
Affiliations
Comment

Facing COVID-19 in the ICU: vascular dysfunction, thrombosis, and dysregulated inflammation

Daniel E Leisman et al. Intensive Care Med. 2020 Jun.
No abstract available

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Conflict of interest statement

ML received research funds from the french ministry of health, research support from Shingotec, lecture fees from Baxter and Fresenius and consulting fees from Novartis. The other authors have no conflict of interest.

Figures

Fig. 1
Fig. 1
(1) The SARS-CoV-2 virus infects an endothelial cell by binding to ACE-2. Cellular infection initiates localized inflammation, endothelial activation, tissue damage, and disordered cytokine release. Membrane fusion also interrupts AngII metabolism, leading to an increase in AngII and a decrease in Ang (1–7), augmenting inflammation, endothelial activation, and leukocyte and platelet recruitment. (2) Pulmonary endothelial activation leads to the ACE-1 shedding phenomenon, where ACE-1 is rapidly liberated from the cell membrane. This produces an initial rapid rise in AngII, which can induce a positive feedback loop enhancing local inflammation, coagulation, and capillary leak. (3) The transiently increased ACE-1 dissipates, leading to subphysiologic AngII concentrations. Low AngII in this phase leads to vasodilation, worsened capillary leak, and impaired endothelial conductance and autoregulation. Low systemic AngII also upregulates ACE-2, possibly increasing susceptibility to SARS-CoV-2 in remote tissue. ACE, angiotensin-converting enzyme; AngI, angiotensin-I; AngII, angiotensin-II; Ang (1–7), angiotensin (1–7); DAMPs, damage-associated molecular pattern molecules
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