Abstract
Trauma or shock is known to produce metabolic changes, anae-robiosis, increased lactate production, a reduction in ATP stores and increase in inorganic phosphate (Kovách et al. 1952). Studies on depression of mitochondrial function in shock are inconclusive. Aldridge and Stoner (1960) found no change in the behaviour of liver mitochondria isolated from rats after limb ischemia. Levenson et al. (1961) reviewing this question concluded that no significant changes in the mitochondrial metabolism in shock could be demonstrated. Fonnesu (1960) demonstrated a partial inhibition of phosphorylation in liver of rats given S. typhi murium toxin. Hift and Strawitz (196l) found normal P/0 ratios in liver mitochondria of dogs in severe hemorrhagic shock. The same observations were made by De Palma et al. (1970) in states where profound ultrastructural changes in mitochondria have been demonstrated (Holden et al. 1965; Strawitz and Hift, 1965).
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These studies were supported by a grant from John A. Hartford Foundation.
Research Fellow, supported by the Heart Association of South Eastern Pennsylvania.
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Kovách, A.G.B., Sándor, P. (1973). Effect of Hemorrhagic Shock on Gluconeogenesis, Oxygen Consumption and Redox State of Perfused Rat Liver. In: Kovách, A.G.B., Stoner, H.B., Spitzer, J.J. (eds) Neurohumoral and Metabolic Aspects of Injury. Advances in Experimental Medicine and Biology, vol 33. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-3228-2_25
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