You are right about the “Dex” crash, it’s coming. I used to climb the largest mountains in the world and one time fell quite ill to H.A.P.E.... took Dexamethasone and felt like Superman for a short period of time... but when it wore off.... oh man
So the possibility exists that since we know now that Leronlimab enters the BBB, this may well be another therapeutic benefit of Leronlimab. Comment from any of our scientists or MD's only please!
Mechanism of Silent Hypoxemia
Given that patients with COVID-19 exhibit several unusual findings, it is possible the virus has an idiosyncratic effect on the respiratory control system.
ACE 2 (angiotensin-converting enzyme 2), the cell receptor of SARS-CoV-2, the virus responsible for COVID-19, is expressed in the carotid body, the site at which chemoreceptors sense oxygen (32). ACE2 receptors are also expressed in nasal mucosa. Anosmia-hyposmia occurs in two-thirds of patients with COVID-19 (33), and the olfactory bulb provides a passage along which certain coronaviruses enter the brain (34). Whether SARS-CoV-2 gains access to the brain through the olfactory bulb and contributes to the association between anosmia-hyposmia and dyspnea (33) and whether ACE2 receptors play a role in the depressed dyspnea response in COVID-19 remain to be determined.
Science (2) links silent hypoxemia with the development of thrombi within the pulmonary vasculature. Increased thrombogenesis has been noted in patients with COVID-19 (35). Thrombi within the pulmonary vasculature can cause severe hypoxemia, and dyspnea is related to pulmonary vascular obstruction and its consequences (36). Dyspnea can also arise from the release of histamine or stimulation of juxtacapillary receptors within the pulmonary vasculature. No biological mechanism exists, however, whereby thrombi in the pulmonary vasculature cause blunting of dyspnea (producing silent hypoxemia). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7397783/
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