Abstract

This preliminary study was undertaken to ascertain whether our newly developed model of the cold ischemic rat liver in situ is applicable to studies designed to assess the metabolism of nutrients. Ischemia of the whole liver of 12 Wistar rats was induced by clamping all supply and drainage vessels. The ischemic liver was perfused in situ. The duration of ischemia of the liver was 20 minutes. Saline was infused into six rats throughout the experiment (group A). An intravenous infusion of glucose at a rate of 0.75 g/h per rat was begun immediately after the induction of blood-reflow to the liver (group B, n = 6). Six rats (group C) did not undergo the procedure for induction of hepatic ischemia and received glucose at the same rate as rats in group B. Changes in hepatic levels of sugar phosphates (phosphomonoesters [PMEs]), inorganic phosphorus, and beta-positioned phosphorus in adenosine triphosphate (beta-ATP) were monitored by 31P magnetic resonance spectroscopy. Ischemia caused a significant increase in levels of PMEs and a decrease in levels of beta-ATP. The infusion of glucose caused a further increase in levels of PMEs and a further decrease in levels of beta-ATP in group B. In contrast, in group C such infusion did not induce any changes in levels of PMEs or beta-ATP. In group A, PMEs and beta-ATP returned to basal levels 5 hours after the induction of blood-reflow to the liver. The changes in levels of PMEs were similar to those in levels of inorganic phosphorus in all groups.(ABSTRACT TRUNCATED AT 250 WORDS)

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