Study sheds light on explanation for lack of blood oxygenation detected in many Covid-19 patients – health


One of the crucial physiopathological characteristics of Covid-19 that has most baffled the scientific and medical community is what is referred to as “silent hypoxemia” or “happy hypoxia”. A recent study sheds light on the explanation for the lack of blood oxygenation detected in many Covid-19 patients.

The study used to be published in the publication operate.

Patients suffering this phenomenon, the causes of which are still unknown, have severe pneumonia with markedly decreased arterial blood oxygen levels (referred to as hypoxemia). Alternatively, they don’t outline dyspnea (subjective feeling of shortness of breath) or increased breathing rates, which are typically characteristic symptoms of people with hypoxemia from pneumonia or any other cause.

Patients with “silent hypoxemia” frequently suffer a sudden imbalance, reaching a critical state that may be fatal. Generally, individuals (healthy or sick) with hypoxemia outline 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 mind to stimulate the respiratory centre.

A group of researchers from the Seville Institute of Biomedicine – IBiS/University Hospitals Virgen del Rocio y Macarena/CSIC/the University of Seville, led by Dr Javier Villadiego, Dr Juan Jose Toledo-Aral and Dr Jose Lopez-Barneo, specialists in the physiopathological study of the carotid body, have suggested in the publication Operate, that “silent hypoxemia” in Covid-19 cases could be caused by this organ being infected by the coronavirus (SARS-CoV-2).

This speculation, which has attracted the interest of the scientific community for its novelty and imaginable therapeutic significance, comes from experiments that have revealed a high presence of the enzyme ECA2, the protein the coronavirus uses to contaminate human cells, in the carotid body. In patients with Covid-19, the coronavirus circulates in the blood. Due to this fact, researchers propose 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. Whether this speculation, which is currently being tested in new experimental models, is confirmed, this would justify using activators of the carotid body independent of the oxygen sensing mechanism as respiratory stimulants in patients with Covid-19.

(This story has been published from a wire agency feed without modifications to the text.)

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