Monoethylglycinexylidide formation as an independent measure of warm hepatic ischemia and reperfusion injury.

An accurate serologic measure of hepatic function would be clinically useful in selecting donors for liver transplantation. An experimental model that incorporates varying lengths of total hepatic warm ischemia with reperfusion injury was utilized to compare serologic parameters and mitochondrial performance of oxidative phosphorylation in predicting hepatocellular injury. Monoethylglycinexylidide (MEGX) formation following bolus intravenous lidocaine injection was found to be significantly decreased (P < 0.0001) at all periods of ischemia when compared to that in nonischemic controls. A serum MEGX level of < 50 micrograms/liter suggested severe hepatic damage. No correlation was found between MEGX level and liver viability as measured by animal survival. Serum transaminase (AST and ALT) levels demonstrated progressive, nonsignificant elevations with increasing length of ischemia (P = 0.0779 at the maximum ischemic time). Polarographic measurements of mitochondrial oxidative phosphorylation did not reveal a significant alteration in subcellular metabolism with prolonged ischemic time. These data highlight the comparative sensitivity of MEGX formation as an early quantitative measurement of hepatocellular injury during warm ischemia, although it was not predictive of organ viability.