Vasile B, Rasulo F, Candiani A, Latronico N. The pathophysiology of propofol infusion syndrome: a simple name for a complex syndrome. Intensive Care Med. 2003 Sep;29(9):1417-25. doi: 10.1007/s00134-003-1905-x. Epub 2003 Aug 6. PMID: 12904852.
https://pubmed.ncbi.nlm.nih.gov/12904852/
As the title mentioned, the article was about pathophysiology, not pathogenesis.
A vicious cycle of catecholamines and propofol is noteworthy, in which, propofol mitigates the efficacy of catecholamines resulting in more requirement of catecholamines, and catecholamines increase cardiac output that mitigates the efficacy of propofol.
Propofol affects mitochondrial function by inhibiting β-spiral oxidation and respiratory chain at complex II
What is β-spiral oxidation
https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/beta-oxidation
three main steps of mitochondrial fatty acid oxidations
1) β-oxidation, where fatty acids undergo oxidative removal of successive two-carbon units as acetyl-CoA, starting at carbon atom 3, the β-carbon of the fatty acyl chain.
4 enzymes: acyl-CoA dehydrogenase, enoyl-CoA hydratase, hydroxyacyl-CoA dehydrogenase and ketoacyl-CoA thiolase.
2) the oxidation of acetyl-CoA to CO2 in the citric acid cycle.
3) flavin adenine dinucleotide and nicotinamide adenine dinucleotide produced during β-oxidation. Electrons derived from the first two steps pass to O2 via the mitochondrial respiratory chain, providing the energy for ATP synthesis by oxidative phosphorylation.
The net yield for the complete oxidation of a palmitic acid molecule is 129 ATP molecules.
