[Investigation of hepatic energy metabolism in normothermic hepatic ischemia--comparison between normal and cirrhotic rat liver].
The purpose of this study was to investigate the energy movement of the normothermic ischemic liver. Liver ischemia was induced in normal and cirrhotic rats, by cross-clamping portal vein and hepatic artery, bypassing the portal blood to the jugular vein through a shunt tube. The levels of ATP of the hepatic tissue was measured before and after hepatic ischemia, by HPLC and 31P-NMR. Before hepatic ischemia, the levels of ATP was greater in normal liver than in cirrhotic liver, but after ischemia it was significantly smaller in normal liver than cirrhotic liver. Generally they say that the greater is the ATP of the tissue, the greater is the viability of the tissue. But this experiment showed the contrary. Cirrhotic liver can't use glucose sufficiently, therefore acetyl-CoA, which is used in TCA-cycle, is derived from the resolution of fatty acid. As a result, free fatty acid and acyl-CoA increase in cirrhotic liver, and suppress Na(+)-K(+)-ATPase. I conclude that the cirrhotic liver can't effectively use ATP to maintain the potential of the liver cells, maybe, because of it's abnormal metabolism of glucose. Therefore, the levels of ATP was greater in cirrhotic liver than in normal liver after hepatic ischemia.
Izu
M
M
First Surgical Department, University of Tokyo, Japan.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D004734:Energy Metabolism; D005947:Glucose / Q000378:metabolism; D006863:Hydrogen-Ion Concentration; D007511:Ischemia / Q000378:metabolism*; D008099:Liver / Q000098:blood supply* / Q000378:metabolism; D008106:Liver Cirrhosis, Experimental / Q000378:metabolism*; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D010758:Phosphorus; D051381:Rats
D010758:Phosphorus; D000255:Adenosine Triphosphate; D005947:Glucose