Oxygen availability, supply, and delivery are not the only fateful factors in providing normal tissue oxygen saturation.
In 1962, Turkington and Nordwind1 were the first to indicate that mitochondria as the main site of respiration and the conservation of oxidate energy through the formation of adenosine triphosphate exert a regulating role on cellular or tissue oxygen metabolism.
In 1973, Goldfischer et al2 reported that they found structural and functional abnormalities in peroxisomes and mitochondria, the two organelles principally concerned with cellular respiration, in patients with cerebral hepatorenal syndrome.
Most recently, Robin3 discussed abnormal tissue oxygen utilization in a special report in the Archives of Internal Medicine. He states that the ultimate cause of the clinical abnormalities associated with changes in oxygen supply and oxygen utilization is the development of abnormal tissue oxygen metabolism. As previous authors have done, he has indicated the cell organelles, especially mitochondria, as
Danilevicius Z. And Now—Dysoxia. JAMA. 1977;238(10):1056. doi:10.1001/jama.1977.03280110060028
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