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10.1016/S2213-2600(21)00213-7 http://scihub22266oqcxt.onion/10.1016/S2213-2600(21)00213-7 34000237!8121498!34000237     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=34000237&cmd=llinks): Failed to open stream: HTTP request failed! 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A tricompartmental model of lung oxygenation disruption to explain pulmonary and systemic pathology in severe COVID-19 |pdf=|usr=}}{{34000237}} gab.com Text A tricompartmental model of lung oxygenation disruption to explain pulmonary and systemic pathology in severe COVID-19 JO: Lancet Respir Med http://www.kidney.de/pget.php?&tw=1&pmid=34000237 #FOAvip The emergent 21st century betacoronaviruses, including SARS-CoV-2, lead to clinicopathological manifestations with unusual features, such as early-onset chest pain, pulmonary infarction, and pulmonary and systemic thromboembolism that is pathologically linked to extensive capillary, arteriolar, and venular thrombosis. Early ground glass opacities detected by CT, which are reminiscent of lung infarcts associated with pulmonary embolism, point to a novel vascular pathology in COVID-19. Under physiological conditions, normal parenchymal oxygenation is maintained by three sources: the alveolus itself and dual oxygen supply from the pulmonary and bronchial artery circulations. We propose a model in which these three components are disrupted in COVID-19 pneumonia, with severe viral alveolitis and concomitant immunothrombotic obstruction of the pulmonary and bronchiolar circulation. Tricompartmental disruption might have two main consequences: systemic clot embolisation from pulmonary vein territory immunothrombosis, and alveolar-capillary barrier disruption with systemic access of thrombogenic viral material. Our model encompasses the known pathological and clinical features of severe COVID-19, and has implications for understanding patient responses to immunomodulatory therapies, which might exert an anti-inflammatory effect within the vascular compartments. Twit Text FOAVip A tricompartmental model of lung oxygenation disruption to explain pulmonary and systemic pathology in severe COVID-19 ????Lancet Respir Med http://www.kidney.de/pget.php?&tw=1&pmid=34000237 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34000237 #FOAvip English Wikipedia <ref>{{Cite pmid|34000237}}</ref> A tricompartmental model of lung oxygenation disruption to explain pulmonary and systemic pathology in severe COVID-19 #MMPMID34000237 McGonagle D; Bridgewood C; Meaney JFM Lancet Respir Med 2021[Jun]; 9 (6): 665-672 PMID34000237show ga The emergent 21st century betacoronaviruses, including SARS-CoV-2, lead to clinicopathological manifestations with unusual features, such as early-onset chest pain, pulmonary infarction, and pulmonary and systemic thromboembolism that is pathologically linked to extensive capillary, arteriolar, and venular thrombosis. Early ground glass opacities detected by CT, which are reminiscent of lung infarcts associated with pulmonary embolism, point to a novel vascular pathology in COVID-19. Under physiological conditions, normal parenchymal oxygenation is maintained by three sources: the alveolus itself and dual oxygen supply from the pulmonary and bronchial artery circulations. We propose a model in which these three components are disrupted in COVID-19 pneumonia, with severe viral alveolitis and concomitant immunothrombotic obstruction of the pulmonary and bronchiolar circulation. Tricompartmental disruption might have two main consequences: systemic clot embolisation from pulmonary vein territory immunothrombosis, and alveolar-capillary barrier disruption with systemic access of thrombogenic viral material. Our model encompasses the known pathological and clinical features of severe COVID-19, and has implications for understanding patient responses to immunomodulatory therapies, which might exert an anti-inflammatory effect within the vascular compartments. |*COVID-19/complications/immunology/physiopathology[MESH] |*Lung/immunology/physiopathology[MESH] |Humans[MESH] |Models, Biological[MESH] |Oxygen Consumption[MESH] |Pulmonary Circulation[MESH] |Pulmonary Embolism/virology[MESH]A tricompartmental model of lung oxygenation disruption to explain pul(epmc).pdf DeepDyve Pubget Overpricing