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.