Document Detail

Sodium bicarbonate treatment during transient or sustained lactic acidemia in normoxic and normotensive rats.
MedLine Citation:
PMID:  23029373     Owner:  NLM     Status:  MEDLINE    
INTRODUCTION: Lactic acidosis is a frequent cause of poor outcome in the intensive care settings. We set up an experimental model of lactic acid infusion in normoxic and normotensive rats to investigate the systemic effects of lactic acidemia per se without the confounding factor of an underlying organic cause of acidosis.
METHODOLOGY: Sprague Dawley rats underwent a primed endovenous infusion of L(+) lactic acid during general anesthesia. Normoxic and normotensive animals were then randomized to the following study groups (n = 8 per group): S) sustained infusion of lactic acid, S+B) sustained infusion+sodium bicarbonate, T) transient infusion, T+B transient infusion+sodium bicarbonate. Hemodynamic, respiratory and acid-base parameters were measured over time. Lactate pharmacokinetics and muscle phosphofructokinase enzyme's activity were also measured.
PRINCIPAL FINDINGS: Following lactic acid infusion blood lactate rose (P<0.05), pH (P<0.05) and strong ion difference (P<0.05) drop. Some rats developed hemodynamic instability during the primed infusion of lactic acid. In the normoxic and normotensive animals bicarbonate treatment normalized pH during sustained infusion of lactic acid (from 7.22 ± 0.02 to 7.36 ± 0.04, P<0.05) while overshoot to alkalemic values when the infusion was transient (from 7.24 ± 0.01 to 7.53 ± 0.03, P<0.05). When acid load was interrupted bicarbonate infusion affected lactate wash-out kinetics (P<0.05) so that blood lactate was higher (2.9 ± 1 mmol/l vs. 1.0 ± 0.2, P<0.05, group T vs. T+B respectively). The activity of phosphofructokinase enzyme was correlated with blood pH (R2 = 0.475, P<0.05).
CONCLUSIONS: pH decreased with acid infusion and rose with bicarbonate administration but the effects of bicarbonate infusion on pH differed under a persistent or transient acid load. Alkalization affected the rate of lactate disposal during the transient acid load.
Franco Valenza; Marta Pizzocri; Valentina Salice; Giorgio Chevallard; Tommaso Fossali; Silvia Coppola; Sara Froio; Federico Polli; Stefano Gatti; Francesco Fortunato; Giacomo P Comi; Luciano Gattinoni
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-09-28
Journal Detail:
Title:  PloS one     Volume:  7     ISSN:  1932-6203     ISO Abbreviation:  PLoS ONE     Publication Date:  2012  
Date Detail:
Created Date:  2012-10-02     Completed Date:  2013-03-05     Revised Date:  2013-07-11    
Medline Journal Info:
Nlm Unique ID:  101285081     Medline TA:  PLoS One     Country:  United States    
Other Details:
Languages:  eng     Pagination:  e46035     Citation Subset:  IM    
Dipartimento di Anestesia, Rianimazione e Terapia del Dolore, Fondazione IRCCS Ca' Granda, Ospedale Maggiore Policlinico, Milan, Italy.
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MeSH Terms
Acidosis, Lactic / blood,  drug therapy*,  enzymology
Hemodynamics / drug effects
Hydrogen-Ion Concentration / drug effects
Lactic Acid / blood
Phosphofructokinases / metabolism
Rats, Sprague-Dawley
Respiratory Rate / drug effects
Sodium Bicarbonate / therapeutic use*
Reg. No./Substance:
144-55-8/Sodium Bicarbonate; 50-21-5/Lactic Acid; EC 2.7.1 -/Phosphofructokinases

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