Mitochondrial Metabolic Alterations in Experimental Circulatory Shock


Lethal endotoxemia induces hypoglycemia, high blood lactate/pyruvate ratios and decreased tissue oxygen utilization. All these metabolic symptoms occur simultaneously. This indicates that the cytoplasmic portion of cellular glucose metabolism, glycolysis, still must be operating, but the mitochondrial reactions, the tricarboxylic acid cycle and/or the electron transfer and oxidative phosphorylation reactions could have become defective. The fact that the gluconeogenetic pathway presumably is inhibited at three different points (5) could explain hypoglycemia and somewhat higher than normal lactate and pyruvate concentrations, but could not count for decreased oxygen utilization. Thus, it was important to us, as well as to some other investigators, to attempt a clarification of possible effects of endotoxemia on mitochondrial metabolic reactions. The importance of these studies is emphasized by the central role of adequate energy production in the survival of cells and vital tissue functions.


Hemorrhagic Shock Liver Mitochondrion Heart Mitochondrion Endotoxic Shock Respiratory Control Ratio 
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© Springer-Verlag/Wien 1975

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  • L. Mela

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