2022-07-052022-07-052013-04-12https://hdl.handle.net/20.500.12503/31317Purpose: Intravenous infusion of sodium pyruvate can protect internal organs from ischemia-reperfusion imposed by cardiac arrest and resuscitation, but may produce hypernatremia due to the sodium load. The purpose of this study was to examine the effects of Na-pyruvate infusion on plasma pyruvate, bicarbonate and sodium concentrations in order to test the hypothesis that pyruvate infusion does not cause persistent hypernatremia. Methods: Swine were subjected to 6 min cardiac arrest, 4 min closed-chest CPR, defibrillation and 4 h recovery. Na-pyruvate (n=7) or NaCl control (n=9) were infused iv (0.1 mmol/kg/min) during CPR and the first 60 min recovery. Results: Pyruvate infusion produced a sustained increase in plasma bicarbonate concentration (44.2 ± 1.2 mM in pyruvate-treated vs. 27.5 ± 2.6 mM in NaCl-treated group at 3 hours post-treatment; P<0.05), which may potentially offset post-arrest acidemia. Although pyruvate and NaCl infusions similarly increased plasma sodium concentrations (146 ± 2 mM and 148 ± l mM, respectively), the hypernatremia resolved to pre-arrest concentrations by 3 h post-pyruvate (140 ± 1 mM), but persisted 3 h post-NaCl (147 ± 2 mM; P<0.05). Conclusions: This study confirms the hypothesis that pyruvate administration after cardiac arrest did not cause persistent hypernatremia.Cardiac ArrestCPRPyruvateposter