It has been established that the anaerobic metabolism in oligemic shock is the product of decreased perfusion through nonvital tissues and is demonstrated by increased blood lactate-pyruvate ratio, and excess lactate as measured by Huckabee.1 This is accompanied by a metabolic acidosis. Attempts at preventing this metabolic acidosis have led to the use of vasodilators to increase nonvital tissue perfusion and buffering systems. Neither of these adjuncts attack the biochemical defect which is the anaerobic production of lactic acid and the disassociation of lactic acid to produce the hydrogen ion. Exton and Park2 demonstrated that the rate of conversion of lactate to glucose is diminished in perfused livers of adrenalectomized rats, and gluconeogenesis is enhanced when exogenous corticosteroids are instilled in the perfusant. This suggests the possibility that corticosteroid-stimulated gluconeogenesis from lactate may be utilized to decrease the amount of lactate in anaerobic tissue. Furthermore, corticoids in pharmacological
Schumer W. Dexamet hasone in Oligemic Shock: Physiochemical Effects in Monkeys. Arch Surg. 1969;98(3):259–261. doi:10.1001/archsurg.1969.01340090035001
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