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The changes in the redox distribution of the ischemic rat liver were studied using the redox scanner, which is a time-sharing, tissue fluorescence and reflectance spectroscopy with fine spatial resolution, with the results presented as a histogram and a gray-scaled picture. Hepatic inflow was clamped for 10 min (group 1), 20 min (group 2), and 30 min (group 3). The ratio of oxidized flavoprotein to reduced pyridine nucleotide fluorescence (FP/PN), representing the intracellular redox state, and hemoglobin reflectance were measured prior to clamping and at subsequent times following declamping in each group. The mean and the range width of FP/PN histogram decreased with the prolongation of ischemic time. In group 1, FP/PN histogram showed a remarkably wide range at 2 min after declamping but was almost completely recovered to preischemic levels at 10 min after declamping. In contrast, in groups 2 and 3, the mean of FP/PN histogram was only partially recovered at 10 min after declamping and the range width continued to increase. The correlation between FP/PN fluorescence and hemoglobin reflectance pictures suggested that the local stagnation of blood flow caused tissue hypoxia, preventing the recovery of the redox state probably in the centrilobular area.
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Kitai et al. (1992) studied this question.
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