Effect of Hemorrhage and Anoxia on Hepatic Gluconeogenesis and Potassium Balance in the Rat

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Abstract
Previous investigations have demonstrated impairment of hepatic gluconeogenic activity during both hypovolemia and sepsis, but the mechanisms responsible remain unclear. The present study was designed to determine the influence of lack of O2 on gluconeogenesis independent of humoral factors, products of ischemic peripheral tissues or pH changes. Livers obtained from Sprague-Dawley rats fasted 24 h were perfused with Krebs-Henseleit buffer containing 5 mM lactate for 30 min. In the control group (n = 8) perfusion was continued; in others, anoxia was induced by perfusing with buffer equilibrated with 95% N2 and 5% CO2 for periods of 15, 30 or 60 min (n = 4, 5 and 5, respectively). The initial conditions were then reinstituted for an additional 45 min. Anoxia caused hepatic release of K+, indicative of disordered hepatic cellular ionic gradients and an abrupt cessation of gluconeogenesis. Reoxygenation partially reversed these alterations but some impairment of gluconeogenesis persisted, and the degree of uptake of K+ from the perfusion media was decreased as the duration of anoxia increased. The degree of restoration of gluconeogenesis after a period of anoxia was closely associated with restoration of cellular uptake of K+. By comparison, livers taken from hypovolemic animals maintained at a mean arterial blood pressure of 40 mm Hg until the beginning of the decompensatory stage of shock exhibited a gluconeogenic capacity of only 41% of control animals, and was comparable to the compromise induced by between 30-60 min of anoxia. The abilities to restore hepatic electrolyte balance and gluconeogenesis after O2 deprivation are apparently affected in parallel and may reflect a common dependence on the restoration of ATP stores after the insult.

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