Liver adenine nucleotide metabolism during ischemia and reperfusion of mice livers studied by phosphorous-31 nuclear magnetic resonance.

Perfusion experiments were performed at 20 degrees C and 37 degrees C to study liver adenine nucleotide metabolism during ischemia and reperfusion of mouse livers using 31P NMR. Perfusing at 8 mL/min (Krebs-Henseleit buffer), ATP was shown to be stable for 6 hours. There was a progressive decrease in the phosphodiesters (glycerophosphorycholine and glycerophosphorylethanolamine) during the 6-hour period. Liver subjected to cold ischemia at 20 degrees C showed a slow decrease in the beta ATP peak during a 42 +/- 6-minute period with a rise in the inorganic phosphate accompanied by a shift of inorganic phosphate to the high field indicating intracellular acidosis. With reperfusion, the beta ATP returned to previous levels and the inorganic phosphate shifted to its original position. During warm ischemia (37 degrees C) the ATP peak disappeared within 5 +/- 1 minute and only returned to 34% of its original value after 30 minutes of ischemia, indicating damage to a certain percentage of liver cells. When the liver was subjected to multiple short periods of cold ischemia, there was complete recovery of the ATP after six cycles. Reperfusion after each period of cold ischemia resulted in an ATP recovery consistently greater than the initial amount, which gradually decreased to preischemic levels after a short period. This suggests that there is an as yet undelineated mechanism of ATP production during ischemia that attempts to protect the cell against ischemia.