Indian Journal of Science and Technology
Year: 2020, Volume: 13, Issue: 30, Pages: 3076-3087
Parthiba Pramanik1, Purushottam Pramanik2*
1Nil Ratan Sirkar Medical College and Hospital, West Bengal, Kolkatta, India
2Department of Zoology, Durgapur Government College, West Bengal, Durgapur, India
Email: [email protected]
Received Date:19 June 2020, Accepted Date:28 July 2020, Published Date:19 August 2020
Background: COVID-19 is the current pandemic infection caused by severe acute respiratory syndrome coronavirus-2 (SARS Cov-2). Pulmonary collapse in severe critical COVID-19 patients may be due to development of multiple micro thrombi within pulmonary vasculature. As COVID-19 pandemic is accelerating, it is important to understand the molecular mechanism through which SARSCov2 induces hypercoagulopathy and intravascular thrombosis to be able to design more appropriate therapy. Focus of this review is to identify mechanisms through re-analysis of publicly available data by which SARS-Cov2 infection induce mortality by augmenting intravascular thrombosis and attempt to understand therapeutic approach to it. Findings: SARS Cov-2 accesses host cells via membrane bound angiotensin converting enzyme-2 (ACE2). This leads to imbalance of renin angiotensin system (RAS) increase ratio of Ag-II: Ag-1-7. Ag-II stimulates release of IP-10 from endothelium which upregulates local renin angiotensin system in endothelial cell by positive feedback process. Therefore it is suggested that angiotensin-II of renin angiotensin systemr in endothelial cells sustained proinflammatory signal and developed microvascular thrombosis. During inflammation both extrinsic and intrinsic coagulation pathways are activated. Fibrinolysis is suppressed by imbalance activity of two system: Ang-II-PAI-1 (plasminigen activator inhibitor-1) and Bradykinin-tPA (tissue plasminogen activator) system. Therapy with low molecular weight heparin (LMWH), which have anticoagulant and anti-inflammatory property, is associated with better prognostic in patients with severe COVID-19. ACE inhibitors decrease production of Ag-II and increases availability of bradykinin and consequence reduces coagulopathy Conclusion: Thus it is concluded that SARS-Cov2 infection induces microvascular thrombosis from hyperinflammation, misbalance between Ag-II and Ag-1-7 and imbalance activity of two system: Ang-II-PAI-1 and bradykinin-tPA system. ACE inhibitor and anticoagulant mainly LMWH and UFH may serve potential role in COVID-19 therapy particularly in patients with hypercoagulopathy and microvascular thrombosis.
Keywords: COVID19; angiotensin converting enzyme; renin angiotensin system; fibrinolysis; microvascular thrombosis; ACE inhibitor; heparin
© 2020 Pramanik & Pramanik.This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Published By Indian Society for Education and Environment (iSee).
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