Cytopathic hypoxia in sepsis: a true problem?
It is increasingly apparent that organ dysfunction in sepsis is caused, at least in part, by an acquired intrinsic derangement in cellular oxidative adenosine triphosphate (ATP) production. We have termed this phenomenon "cytopathic hypoxia". Although several different but mutually compatible mechanisms might account for the development of cytopathic hypoxia in sepsis, recent data from our laboratory point to activation of the nuclear enzyme, poly-ADP-ribosyl polymerase (PARP), as being the most important.
Fink
M P
MP
University of Pittsburgh Medical School, Division of Critical Care Medicine, Anesthesiology and Critical Care Medicine, 3550 Terrace Street, Room 616 Scaife Hall, Pittsburgh, PA 15261, USA. finkmp@anes.upmc.edu
D000244:Adenosine Diphosphate / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism*; D000332:Aerobiosis; D000818:Animals; D015687:Cell Hypoxia; D004789:Enzyme Activation; D005182:Flavin-Adenine Dinucleotide / Q000031:analogs & derivatives* / Q000378:metabolism; D006801:Humans; D008928:Mitochondria / Q000378:metabolism; D009243:NAD / Q000378:metabolism; D010766:Phosphorylation; D011065:Poly(ADP-ribose) Polymerases / Q000378:metabolism*; D018805:Sepsis / Q000378:metabolism* / Q000503:physiopathology
D009243:NAD; D005182:Flavin-Adenine Dinucleotide; C058805:1,5-dihydro-FAD; D000244:Adenosine Diphosphate; D000255:Adenosine Triphosphate; D011065:Poly(ADP-ribose) Polymerases