Failure of an increased dose of ATP-MgCl2 to improve protein synthesis and transmembrane potential in the postischemic liver.
To study the effects of ATP-MgCl2 on impaired protein synthesis and hepatic cell membrane potential (HCMP) in the postischemic liver, ATP-MgCl2 (50 or 150 mumole/kg) or saline was administered intravenously following 90 min of liver ischemia in rats. Protein synthesis was measured by determining rate of leucine incorporation into proteins in incubated liver slices. HCMP was registered in vivo with glass microelectrodes. No effects of the two doses of ATP-MgCl2 on protein synthesis or HCMP in the postischemic liver were found. The results indicate that beneficial effects of ATP-MgCl2 previously reported following liver ischemia are not primarily caused by direct energy provision to hepatocytes.
D000136:Acid-Base Equilibrium / Q000187:drug effects; D000255:Adenosine Triphosphate / Q000494:pharmacology*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D007511:Ischemia / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008102:Liver Circulation; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D014176:Protein Biosynthesis; D051381:Rats; D011919:Rats, Inbred Strains
D000255:Adenosine Triphosphate