id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-355208-hpldjsc5	Leisman, Daniel E.	Facing COVID-19 in the ICU: vascular dysfunction, thrombosis, and dysregulated inflammation	2020-04-28		.txt	text/plain	1414	93	35	The reported inflammatory response in COVID-19 is also not consistent with either typical ARDS or cytokine-release syndromes (CRS) or "cytokine storm. Reports of increased respiratory dead space suggest lung-vascular thrombosis from thrombotic microangiopathy or pulmonary embolism. Reported findings indicate that immunosuppression, endothelial activation, and direct viral-mediated tissue damage, rather than hyperinflammatory injury, mediate COVID-induced organ dysfunction. Viral injury, disordered cytokine release, and damage-associated 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. ACE, angiotensin-converting enzyme; AngI, angiotensin-I; AngII, angiotensin-II; Ang (1-7), angiotensin (1-7); DAMPs, damage-associated molecular pattern molecules molecular patterns (DAMPs) induce localized microvascular inflammation, which triggers endothelial activation, leading to vasodilation and pro-thrombotic conditions. Among the known effects of AngII are vasoconstriction, endothelial activation, and pro-inflammatory cytokine release. COVID-induced respiratory failure involves physiologic, clinical, and immunologic phenotypes that are not consistent with either ARDS or cytokine-release syndromes.	./cache/cord-355208-hpldjsc5.txt	./txt/cord-355208-hpldjsc5.txt