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Intravenous Pyruvate for Cardiac Arrest Does Not Cause Persistent Hypernatremia
Author(s) -
Cherry Brandon Hunter,
Nguyen Anh Q,
Ryou MyoungGwi,
Williams Arthur,
Hoxha Besim,
OlivenciaYurvati Albert H,
Mallet Robert T
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1206.6
Subject(s) - hypernatremia , sodium pyruvate , sodium bicarbonate , medicine , resuscitation , sodium , pyruvate dehydrogenase complex , anesthesia , endocrinology , chemistry , biochemistry , organic chemistry , enzyme
Intravenous infusion of sodium pyruvate can protect internal organs from ischemia‐reperfusion injury imposed by cardiac arrest and resuscitation, but this treatment may impose hypernatremia due to the sodium load. Here, the effect of sodium pyruvate infusion on plasma pyruvate, bicarbonate and sodium concentrations were assessed in Yorkshire swine subjected to cardiac arrest, closed‐chest CPR, defibrillation and recovery. Na pyruvate (n=7) or equimolar NaCl control (n=9) were infused iv during CPR and the first 60 min recovery. Table (mM; mean ± SEM; *P < 0.05 v. NaCl): Pyruvate and NaCl infusions similarly increased plasma sodium concentrations; the hypernatremia resolved by 3 h post‐pyruvate, but persisted 3 h post‐NaCl. Pyruvate infusion produced a sustained increase in bicarbonate concentration, which could potentially offset post‐arrest acidemia. Thus, pyruvate administration following cardiac arrest did not cause persistent hypernatremia.