Depletion of replenishment of cellular cyclic adenosine monophosphate in hemorrhagic shock.
Hemorrhagic shock in rats was produced by bleeding them to a mean arterial blood pressure of 40 millimeters of mercury, which was maintained for two hours. After sacrifice, small pieces of liver, kidney, muscle and brain were quickly removed and frozen in liquid nitrogen. A protein-free extract of tissues was prepared, and cyclic adenosine monophosphate was measured by the radioimmunoassay procedure. Analysis os liver, kidney, muscle and brain showed that there were significant reductions in cyclic adenosine monophosphate and adenosine triphosphate levels. The decrease in cyclic adenosine monophosphate levels follow the same trend in the various organs as the decreases in adenosine triphosphate levels, suggesting that these two events are related. Infusion of adenosine triphosphate-magnesium chloride, 25 micromoles each, at the end of the shock period restored the cellular cyclic adenosine monophosphate and adenosine triphosphate levels. The precise mechanism for depletion and replenishment of cyclic adenosine monophosphate levels during shock is not now known.
D000255:Adenosine Triphosphate / Q000378:metabolism / Q000627:therapeutic use; D000818:Animals; D001921:Brain / Q000378:metabolism; D002712:Chlorides / Q000627:therapeutic use; D000242:Cyclic AMP / Q000378:metabolism*; D007668:Kidney / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008274:Magnesium / Q000627:therapeutic use; D009132:Muscles / Q000378:metabolism; D051381:Rats; D012771:Shock, Hemorrhagic / Q000188:drug therapy / Q000378:metabolism*
D002712:Chlorides; D000255:Adenosine Triphosphate; D000242:Cyclic AMP; D008274:Magnesium