J.Jpn. Surg. Soc.. 88(9): 1196-1199, 1987

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Report on the annual meeting

STUDIES ON PATHOGENESIS AND EFFECTS OF GLUCOCORTICOID IN ENDOTOXIN SHOCK

In septic shock, accelerated glycolysis occurs and may either be associated with rapid glycogen mobilization or with compensatory changes in glucoregulatory enzymes. This possibility was investigated using glucoregulatory enzymes and TCA cycle activity of liver slices from fasted rats after inducing peritonitis by cecal incision. Liver samples were taken at 3 and 5h. These samples free ofmitochondria were assayed by UV Spectrophotometry for phosphofructokinase (PFKase), pyruvatekinase (PKase), glucose-6-phosphatase (G6Pase), fructose-1.6-diphosphatase (FDPase), and phosphoenolpyruvate carboxykinase (PEPCK). The liver slices held medium solution plus ¹⁴C-glucose, ¹⁴C-glutamate or ¹⁴C-pyruvate and were gassed with 95％ O₂-5％ CO₂ gas mixture. The reaction allowed to continue for two hours. Incorporation rate was calculated from the formula. Although at 5h septic PFKase was 22.3±2.9 U/g protein/min and PKase was 252±32, these enzymes were significantly stimulated 13％ and 14％, respectively. No other differences were noted. The rate of TCA cycle activity was significantly decreased 55％ in the septic 5h group. Thus an increase in glycolysis was a common finding in septic shock and was an apparent compensatory reaction for diminished mitochondrial TCA cycle function. When glucocorticoid was given IV at the time of cecal incision, PFKase, PKase, G6Pase and PEPCK were stimulated, respectively. The rate of TCA cycle activity was significantly increased. Thus the possibility that protective glucocorticoids prevent the proteolytic catabolism of glycolytic enzymes must also be considered.

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