Effects of B-Blockers on the Sympathetic and Cytokines Storms in Covid-19.
Date
2021
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Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a causative virus in the development of coronavirus disease 2019 (Covid-19) pandemic. Respiratory manifestations of SARS-CoV-2 infection such as acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) leads to hypoxia, oxidative stress, and sympatho-activation and in severe cases leads to sympathetic storm (SS). On the other
hand, an exaggerated immune response to the SARS-CoV-2 invasion may lead to
uncontrolled release of pro-inflammatory cytokine development of cytokine storm (CS).
In Covid-19, there are interactive interactions between CS and SS in the development of
multi-organ failure (MOF). Interestingly, cutting the bridge between CS and SS by antiinflammatory
and anti-adrenergic agents may mitigate complications that are induced by
SARS-CoV-2 infection in severely affected Covid-19 patients. The potential mechanisms
of SS in Covid-19 are through different pathways such as hypoxia, which activate the
central sympathetic center through carotid bodies chemosensory input and induced proinflammatory
cytokines, which cross the blood-brain barrier and activation of the sympathetic center. b2-receptors signaling pathway play a crucial role in the production of pro-inflammatory cytokines, macrophage activation, and B-cells for the production of antibodies with inflammation exacerbation. b-blockers have anti-inflammatory effects through reduction release of pro-inflammatory cytokines with inhibition of NF-kB. In conclusion, b-blockers interrupt this interaction through inhibition of several mediators of CS and SS with prevention development of neural-cytokine loop in SARS-CoV-2 infection. Evidence from this study triggers an idea for future prospective studies to confirm the potential role of b-blockers in the management of Covid-19.
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Keywords
B-Blockers, Sympathetic, Cytokines, Storms, Covid-19