COVID-19 Research: Silent Hypoxemia Detected In Numerous COVID-19 Patients Is Possibly Due to Carotid Bodies Being Infected by SARS-CoV-2
Source: COVID-19 Research Dec 30, 2020 3 years, 10 months, 3 weeks, 2 days, 15 hours, 9 minutes ago
COVID-19 Research: A new study by researchers from the Seville Institute of Biomedicine-Spain, the University Hospitals Virgen del Rocío y Macarena-Spain and University of Seville-Spain have found that silent hypoxemia or the lack of blood oxygenation detected in numerous COVID-19 patients is possibly due to carotid bodies being infected by the SARS-CoV-2 coronavirus.
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The carotid bodies (CB) are chemoreceptors located in the adventitia of the bifurcation of the common carotid artery. The main chemoreceptor functions of these carotid bodies are to monitors the blood's pH, pCO2, and pO2 and thereby modulates cardiovascular and respiratory function primarily through sympathetic tone.
When these carotid bodies are infected by the SARS-CoV-2 coronavirus, their functions are disrupted leading to the issue of silent hypoxemia. According to the study team, bilateral removal of the CB in humans leaves individuals unaware of hypoxemia, with complete abolition of the hypoxic ventilatory response.
Therefore, inhibition of CB responsiveness to hypoxia could be a plausible explanation for the impaired respiratory drive and reduced dyspnea that characterizes the “silent hypoxemia” observed in COVID-19 patients.
The study findings were published in the peer reviewed journal: Function.
https://academic.oup.com/function/article/2/1/zqaa032/5998649
To date, one of the physiopathological characteristics of COVID-19 that has most baffled the scientific and medical community is what is known as "silent hypoxemia," or "happy hypoxia."
COVID-19 patients suffering this phenomenon, the causes of which are still unknown, have severe pneumonia with markedly decreased arterial blood oxygen levels (known as hypoxemia). However, they do not report dyspnea (subjective feeling of shortness of breath) or increased breathing rates, which are usually characteristic symptoms of people with hypoxemia from pneumonia or any other cause.
Most COVID-19 patients with "silent hypoxemia" often suffer a sudden imbalance, reaching a critical state that can be fatal. Normally, individuals (healthy or sick) with hypoxemia report a feeling of shortness of breath and a higher breathing rate, thus increasing the body's uptake of oxygen. This reflex mechanism depends on the carotid bodies. These small organs, located on either side of the neck next to the carotid artery, detect the drop in blood oxygen and send signals to the brain to stimulate the respiratory centre.
The study team led by Dr Javier Villadiego, Dr Juan José Toledo-Aral and Dr José López-Barneo, specialists in the physiopathological study of the carotid body, have suggested that "silent hypoxemia" in COVID-19 cases could be caused by the carotid body being infected by the coronavirus (SARS-CoV-2).
This new hypothesis, which has attracted the interest of the scientific community for its novelty and possible therapeutic significance, comes from experiments that have revealed a high presence of the enzyme ECA2, the protein the coronavirus uses to infect human cells, in the carot
id body.
In patients with COVID-19, the coronavirus circulates in the blood. Therefore, researchers suggest that infection of the human carotid body by SARS-CoV-2 in the early stages of the disease could alter its ability to detect blood oxygen levels, resulting in an inability to "notice" the drop in oxygen in the arteries. If this hypothesis, which is currently being tested in new experimental models, is confirmed, this would justify the use of activators of the carotid body independent of the oxygen sensing mechanism as respiratory stimulants in patients with COVID-19.
The study team concluded, “We suggest that SARS-CoV-2 CB infection could be the cause of, or contribute to, the “silent hypoxemia” observed in COVID-19 patients. Our proposal could be tested in autopsy studies of CB tissue obtained from COVID-19 patients and by experimental work using humanized ACE2-mouse transgenic models. In addition, if our hypothesis is correct, it would be necessary to study whether or not the damage produced by SARS-CoV-2 infection in the chemosensitive CB tissue is transient and to what extent it alters the regenerative potential of CB stem cells. If confirmed, our hypothesis would warrant the use of CB activators as respiratory stimulants in COVID-19 patients. These drugs act downstream the mitochondrial O2 sensor as they directly block K+ channels in glomus cells.”
https://pubmed.ncbi.nlm.nih.gov/31618601/
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