Effects of B-Blockers on the Sympathetic and Cytokines Storms in Covid-19.
| dc.contributor.author | Al-kuraishy, Hayder M. | |
| dc.contributor.author | Al-Gareeb, Ali Ismail | |
| dc.contributor.author | Mostafa-Hedeab, Gomaa | |
| dc.contributor.author | Keneth Iceland, Kasozi | |
| dc.contributor.author | Zirintunda, Gerald | |
| dc.contributor.author | Aslam, Akhmed | |
| dc.contributor.author | Allahyani, Mamdouh | |
| dc.contributor.author | Welburn, Susan Christina | |
| dc.contributor.author | Batiha, Gaber El-Saber | |
| dc.date.accessioned | 2023-01-31T12:21:24Z | |
| dc.date.available | 2023-01-31T12:21:24Z | |
| dc.date.issued | 2021 | |
| dc.description.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. | en_US |
| dc.identifier.uri | http://hdl.handle.net/20.500.12493/906 | |
| dc.language.iso | en_US | en_US |
| dc.subject | B-Blockers | en_US |
| dc.subject | Sympathetic | en_US |
| dc.subject | Cytokines | en_US |
| dc.subject | Storms | en_US |
| dc.subject | Covid-19 | en_US |
| dc.title | Effects of B-Blockers on the Sympathetic and Cytokines Storms in Covid-19. | en_US |
| dc.type | Article | en_US |