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10.1016/j.mehy.2020.110039

http://scihub22266oqcxt.onion/10.1016/j.mehy.2020.110039
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32758881!7834242!32758881
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suck abstract from ncbi


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pmid32758881      Med+Hypotheses 2020 ; 144 (ä): 110039
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  • SARS-CoV-2 and the sympathetic immune response: Dampening inflammation with antihypertensive drugs (Clonidine and Propranolol) #MMPMID32758881
  • Hyoju SK; Zaborina O; van Goor H
  • Med Hypotheses 2020[Nov]; 144 (ä): 110039 PMID32758881show ga
  • Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is now a pandemic with the United States now carrying the highest number of cases and fatalities. Although vaccines and antiviral agents are the main focus of therapy, here we present a plausible hypothesis to leverage our understanding of neuroimmunomodulation to intervene in the pathophysiology of the disease to prevent death.
  • |Antihypertensive Agents/*therapeutic use[MESH]
  • |Antiviral Agents/therapeutic use[MESH]
  • |COVID-19/*immunology/virology[MESH]
  • |Clonidine/*therapeutic use[MESH]
  • |Comorbidity[MESH]
  • |Disease Progression[MESH]
  • |Humans[MESH]
  • |Immune System/*virology[MESH]
  • |Inflammation/*virology[MESH]
  • |Interleukin-6/blood[MESH]
  • |Models, Theoretical[MESH]
  • |Myocardium/pathology[MESH]
  • |Propranolol/*therapeutic use[MESH]
  • |Randomized Controlled Trials as Topic[MESH]


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