Y Mimura1, K Furuya. 1. Third Department of Surgery, University of Tokyo, Japan.
Abstract
BACKGROUND: Oxygen supply to the tissues is needed in the early postoperative period to meet the energy requirements for maintaining cellular activity. This study was done to investigate energy metabolism in rats during hypoxia in order to determine the mechanism underlying the acclimatization of energy production to oxygen depletion. STUDY DESIGN: Wistar rats were divided into two experimental groups: hypoxic and normoxic, which were supplied with 10 and 21 percent oxygen for 20 hours, respectively. At the end of the experiment, blood and hepatic tissue samples were taken to determine endocrine and metabolic responses to hypoxia. Energy expenditure during hypoxia was also evaluated. RESULTS: Hypoxia resulted in marked increases in blood concentrations of triglycerides, free fatty acids, catecholamines, and corticosterone. Hypoxia marked by depressed resting energy expenditure and respiratory quotient, and produced a stable hepatic adenosine triphosphate (ATP) level. The cytosolic redox state, represented by the ratio of lactate to pyruvate concentrations in the liver, and the arterial ketone body ratio declined during hypoxia. With hypoxia, an increase in alanine and decreases in glutamine and glutamate levels in the liver were observed. CONCLUSIONS: These results suggest that hypoxia depresses energy expenditure, which leads to a normoxic level of hepatic ATP. Fat is a main metabolic fuel during hypoxia. Hypoxia leads to the development of a pathway that shunts pyruvate and glutamate to alanine and alpha-ketoglutarate, allowing efficient energy production.
BACKGROUND:Oxygen supply to the tissues is needed in the early postoperative period to meet the energy requirements for maintaining cellular activity. This study was done to investigate energy metabolism in rats during hypoxia in order to determine the mechanism underlying the acclimatization of energy production to oxygen depletion. STUDY DESIGN:Wistar rats were divided into two experimental groups: hypoxic and normoxic, which were supplied with 10 and 21 percent oxygen for 20 hours, respectively. At the end of the experiment, blood and hepatic tissue samples were taken to determine endocrine and metabolic responses to hypoxia. Energy expenditure during hypoxia was also evaluated. RESULTS:Hypoxia resulted in marked increases in blood concentrations of triglycerides, free fatty acids, catecholamines, and corticosterone. Hypoxia marked by depressed resting energy expenditure and respiratory quotient, and produced a stable hepatic adenosine triphosphate (ATP) level. The cytosolic redox state, represented by the ratio of lactate to pyruvate concentrations in the liver, and the arterial ketone body ratio declined during hypoxia. With hypoxia, an increase in alanine and decreases in glutamine and glutamate levels in the liver were observed. CONCLUSIONS: These results suggest that hypoxia depresses energy expenditure, which leads to a normoxic level of hepatic ATP. Fat is a main metabolic fuel during hypoxia. Hypoxia leads to the development of a pathway that shunts pyruvate and glutamate to alanine and alpha-ketoglutarate, allowing efficient energy production.
Authors: Fernando D Saraví; Daniel R Chirino; Teobaldo A Saldeña; Liliana M Cincunegui; Graciela E Carra; Leonor M E Ituarte Journal: Dig Dis Sci Date: 2002-05 Impact factor: 3.199
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