Ethanol Intoxication and Lactated Ringer's Resuscitation Prolong Hemorrhage-Induced Lactic Acidosis

Abstract

Ethanol (EtOH) blunts the respiratory and metabolic compensation during hemorrhage, resulting in a more severe lactic acidemia. We hypothesized that lactated Ringer's (LR) resuscitation may exacerbate this lactic acidemia. Male guinea pigs were implanted with arterial and venous catheters. Two days after catheter placement, conscious animals were injected intraperitoneally with 1 g/kg EtOH, 0.3 g/kg EtOH, or an equal volume of water 30 min before hemorrhage (60% of estimated blood volume). After 30 min of hemorrhagic shock, animals were resuscitated with isotonic saline (S) or LR at 1 mL/min (three times shed blood volume). Mean arterial blood pressure (MABP) was not affected by pretreatment with either dose of EtOH, but was significantly decreased by hemorrhage in all groups. Both S and LR resuscitation slightly increased MABP, but neither restored it to prehemorrhage values. Blood lactate levels increased in all groups during hemorrhage and remained elevated for 3 h in animals pretreated with 1 g/kg EtOH. In the group pretreated with 0.3 g/kg EtOH, pH decreased during shock but returned to prehemorrhage levels during the resuscitation period. Resuscitation with S returned pH to prehemorrhage values in animals pretreated with 1.0 g/kg EtOH. Resuscitation with LR did not exacerbate, but did prolong, the lactic acidemia after shock in animals pretreated with 1.0 g/kg EtOH. Administration of additional lactate during intoxication and hypovolemia for hemodynamic stabilization before blood transfusion may exacerbate a metabolic stress.

Pyruvate in the Correction of Intracellular Acidosis: A Metabolic Basis as a Novel Superior Buffer

“…Although sodium Lac itself is almost obsolete in the treatment of clinical acidosis, several recent studies have demonstrated that lactated Ringer’s solution (28 m M ) was beneficial in the resuscitation of massive hemorrhagic shock accompanied with lactic acidosis. It significantly improved acidosis and survival rates [17,21,22,23]. In rat working hearts after hemorrhagic shock accompanied with lactic acidosis and impaired PDC activities, Lac at 8.0 m M in the presence of palmitate in perfusates saturated with 95% oxygen improved cardiac efficiency [21].…”

“…Most likely the intracellular acidosis was attenuated although pHi data were not determined. The paradoxical effect of exogenous Lac on experimental lactic acidosis above has not been fully interpreted, but may be associated with several reasons: different species of models, early stage of shock, over 40 mm Hg of mean arterial pressure of shock and anesthesia conditions [17,21,22,23]. The above findings indicated that the TCA cycle function in vital organs remained, at least partially, intact for Lac oxidation [24].…”

“…Further, a recent clinical investigation found that in patients with early postoperative cardiogenic shock accompanied with lactic acidosis, the clearance of exogenous Lac was not significantly altered, compared with controls [30]. In contrast, if shock despite causes in origin are severe [31] or combined with alcoholic intoxication [23], preexisting liver diseases, diabetes or multiple organ injuries, the Lac infusion most likely exacerbates lactic acidosis. Therefore, it should be taken into account in the deduction of Lac effects on acidosis in above-mentioned experimental results if the oxidative phosphorylation of TCA cycle or gluconeogenesis in vital organs was, at least in part, sustained during early shock (hypoxia) or recovered after shock (reoxygenation).…”