Respiration and Glycolysis of Liver Slices From Normal and Shocked Rats Subjected to Food and Water Deprivation

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Abstract
The effects of food and water deprivation in normal and shocked rats were studied with reference to their influence on the in vitro Q02 of liver tissue. An increase in the tissue Q02 was found when the well-fed rat was subjected to 24-30 hour intervals of fasting or to ischemic shock. This increase was found to be referable to a decrease in the tissue glycogen content. The increased respiration following ischemic shock approximated that following the fasting interval. In the normal rat fasting intervals longer than 24-30 hours led to decreasing QO2 values. Liver QO2 values unchanged from that shown by the control tissues were usually found in ischemic shock rats that had been fasted for 24-30 hours. A decrease in the liver QO2 was usually found when animals in ischemic shock were subjected to a 36-42 hour fast. Furthermore, a decrease was always found when the rats were subjected to water deprivation during the ischemia and shock in the 24-30 hour fasted rat. Finally, a very marked decrease in the liver QO2 was found when the 24-30 hour fasted rats were subjected to nemorrhagic rather than ischemic shock. The effect of hemorrhagic shock on the metabolism of rat liver slices was investigated with reference to the aerobic and anaerobic phases of glucose catabolism. The rate of anaerobic glycolysis in tissue from these animals was greater than that in normal tissue when glucose was used as substrate, but is unchanged from the normal values when hexosediphosphate or glucose in the presence of 0.01 [image] K ion were utilized as substrates. When glucose, pyruvate, acetoacetate, acetate, citrate or glutamate were utilized as substrates the rate of O2 consumption was always depressed in the shocked tissue. A structural or chemical derangement in the mitochondria of liver tissue was discussed as an hypothesis to explain the depression in glucose catabolism during shock.