A response of the immune system is triggered when SARS-CoV-2 is transmitted, which tries to prevent the illness from progressing. However, severe COVID-19 may cause a number of side effects, including ARDS and organ failure, in reaction to the high rate of replication of the virus. Initial tissue damage resulting from a SARS-CoV-2 infection causes the production of cytokines, signaling molecules. Damaged tissues produce cytokines and other chemicals that are recruited by immune cells like neutrophils and macrophages, resulting in their activation. ARDS (acute respiratory distress syndrome) is characterized by overactivation of neutrophils and macrophages, and cytokine storm, a medical term for excessive cytokine synthesis. Scientists attribute COVID-19 to ARDS. The recruited neutrophils and macrophages generate cytokines and contribute to the cytokine storm itself, which occurs when active neutrophils and macrophages are present in the lungs. Activated neutrophils further launch granules and manufacture NETs that are deadly to pathogens. NETs are web-like structures that immobilize bacteria and viruses using DNA and proteins. Hyperactivation of neutrophils, although it serves an important function in fighting the virus, also results in lung tissue and blood vessel damage, as seen in ARDS. Neutrophils seen in the lungs are a good indicator of the severity of COVID-19 and are connected to complications such as ARDS. These results support the notion that neutrophils may be a great choice for helping reduce lung inflammation in individuals with significant (or severe) inflammation. COVID-19.
The two hormones that fight-or-flight relies on are adrenaline and norepinephrine, and medicines of the Beta-blocker class inhibit the effects of those hormones. People with heart problems take beta-blockers, a popular medication.
Dr. Kjeldsen’s article last year said that beta-blockers, because of their capacity to decrease inflammation and fight fluid buildup in the lungs, were potential therapeutic options for individuals with severe COVID-19. Now researchers at the Carlos III National Cardiovascular Research Center (CNIC) have discovered that the beta-blocker metoprolol improves blood oxygen levels and also reduces lung inflammation. ARDS patients participating in a short trial performed with COVID-19 were studied to get these findings. The researchers discovered that, for example, metoprolol resulted in a lower neutrophil count in the lungs and a lower neutrophil activation level.
The co-author of the study Dr Valentin Fuster, CNIC Director General and Mount Sinai Heart Director, told MNT: “We have very little treatment that has shown to be of importance to us at this late stage of the illness. This research has shown that with the use of a new inexpensive and easily available medication, we can tackle a problem that has been overlooked for too long.