ATP-MgCl2 treatment prior to hypoxic-hypotension.
We have previously implicated uncoupling of oxidative phosphorylation and the associated decreased concentrations of tissue adenosine triphosphate (ATP) in the liver and brain as major factors contributing to death after hypoxia and hypotension. To determine if intravenously administered ATP-MgCl2 complex would result in increased liver and/or brain concentration of ATP, rats were pretreated with intravenous ATP-MgCl2 prior to exposing them to hypoxic-hypotensive stress. In this preliminary work, pretreatment was selected based on the premise that such an experimental design was most apt to demonstrate an effect if such existed. Baseline cerebral cortical and liver ATP and lactate concentrations were obtained immediately after the intravenous infusion of either saline (control group) or ATP-MgCl2 (treated group). ATP and lactate concentrations were again determined after 30 min hypoxic-hypotension and 20 min after resuscitation. ATP-MgCl2 pretreatment resulted in a modest increase in hepatic ATP concentration when measured after 30 min of hypoxic-hypotension. This increase was not evident 20 min later. No increases in cerebral ATP concentrations were noted at any sample time after ATP-MgCl2 pretreatment.
D000255:Adenosine Triphosphate / Q000494:pharmacology*; D000818:Animals; D001923:Brain Chemistry; D002712:Chlorides / Q000494:pharmacology; D007022:Hypotension / Q000378:metabolism*; D000860:Hypoxia / Q000378:metabolism*; D008099:Liver / Q000032:analysis; D008274:Magnesium / Q000494:pharmacology*; D008297:Male; D051381:Rats; D012771:Shock, Hemorrhagic / Q000378:metabolism / Q000503:physiopathology*
D002712:Chlorides; D000255:Adenosine Triphosphate; D008274:Magnesium