Siddiqi et al. wrote in January 2021,
Pulmonary ECs [= endothelial cells, in this paper] have an important role in immune surveillance, maintaining alveolar integrity and ensuring appropriate oxygen exchange. In COVID-19, direct viral infection and the systemic inflammatory response likely lead to severe dysfunction of these important ECs, compounding the resulting picture of severe hypoxia and acute respiratory distress syndrome frequently reported in hospitalized patients.
Question: does COVID infection of other endothelial cells interfere with internal respiration (oxygen and/or possibly CO2 exchange at the destination tissues)?
I find some of the responses confusing. The quoted text says that pulmonary endothelial cells have a role in ensuring appropriate oxygen exchange - this is no surprise since the oxygen passes through the cells. "Oxygen permeability" refers to how well the oxygen passes through the cells. "Internal respiration" is the anatomical term for the exchange of gases at the systemic capillaries. The mechanism of action, as stated in the quote, is a combination of direct viral infection and systemic inflammatory response - I expect more the latter. Whether COVID infects the endothelial cell directly, affects a neighboring cell, or causes differences in serum cytokines that affect the endothelial cells, all I was wondering is whether as a whole, the wall of an infected person's systemic capillary would diffuse oxygen more slowly.