Liver viability after ischemia-reperfusion
A. A. Rodriguez, W. W. LaMorte, L. M. Hanrahan, S. R. Hopkins, J. C. O'Keane, R. Cachecho and E. F. Hirsch
Department of Surgery, Sears Surgical Laboratory, Boston University School of Medicine, MA 02118.
Lack of a reproducible model to quantitatively assess hepatocellular injury
following ischemia has made it difficult to assess new strategies for
minimizing hepatic injury. We studied the progression of hepatocellular
injury after ischemia and ischemia with reperfusion in rats. Irreversible
injury was quantitated using a triphenyltetrazolium chloride assay that was
shown to correlate with ultrastructural changes. Adenosine triphosphate
decreased to 36% of basal values after 30 minutes, but returned to normal
with reperfusion with no decrease in viability. In contrast, viability fell
by 30% after 60 minutes of ischemia, and by 64% when 60 minutes of ischemia
was followed by reperfusion. We conclude that reperfusion of ischemic liver
increases the degree of irreversible damage. The model employed here seems
to be useful for studying ischemic and reperfusion injury in the liver.
