The effects of iv sodium bicarbonate (NaHCO3) and Carbicarb, an experimental buffer, were compared in a rat model of lactic acidosis induced by controlled hemorrhage and asphyxia. Although both NaHCO3 and Carbicarb were effective at alkalinizing the arterial blood in this model, NaHCO3 administration resulted in a rise in PaCO2 where Carbicarb did not (+9 +/- 2 vs. +2 +/- 2 torr at 2 min after infusion, p less than .01). Moreover, NaHCO3 resulted in a small decrease in intracellular brain pH as measured with P-31 nuclear magnetic resonance where Carbicarb afforded intracellular brain alkalinization (-0.03 +/- 0.01 vs. +0.08 +/- 0.02 pH units at 2 min, p less than .01). If these data are confirmed clinically, Carbicarb may offer advantages over NaHCO3 under conditions of fixed or limited ventilation.
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http://dx.doi.org/10.1097/00003246-198912000-00015 | DOI Listing |
Acidification of the cellular lysosome is an important factor in infection of mammalian cells by SARS-CoV-2. Therefore, raising the pH of the lysosome would theoretically be beneficial in prevention or treatment of SARS-CoV-2 infection. Sodium bicarbonate, carbicarb, and THAM are buffers that can be used clinically to provide base to patients.
View Article and Find Full Text PDFAm J Kidney Dis
September 2016
Department of Medicine, Division of Nephrology, St. Elizabeth's Medical Center, Boston, MA; Department of Medicine, Tufts University School of Medicine, Boston, MA. Electronic address:
Mortality rates associated with severe lactic acidosis (blood pH<7.2) due to sepsis or low-flow states are high. Eliminating the triggering conditions remains the most effective therapy.
View Article and Find Full Text PDFLactic acidosis (LA) is the most common form of metabolic acidosis defined by values of lactate greater than 5 mmol / l and by a pH <7.34. The pathogenesis of LA involves hypoxic (type A) and non hypoxic (type B) causes which are often coexisting.
View Article and Find Full Text PDFClin Chim Acta
May 2006
Department of Physiology, Dr. A.L.M. Postgraduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai-600113, TamilNadu, India.
Background: Formic acid is a toxic metabolite responsible for the metabolic acidosis in methanol poisoning. Formate dehydrogenase (EC 1.2.
View Article and Find Full Text PDFToxicol Lett
February 2006
Department of Physiology, Dr. A.L.M. Postgraduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai 600113, Tamil Nadu, India.
Methanol remains to be a major public and environmental health hazard. Formic acid is the toxic metabolite responsible for the metabolic acidosis observed in methanol poisoning in humans, in non-human primates and in folate-depleted rodents. Cytochrome oxidase inhibition by formate leads to lactic acid accumulation, which contributes significantly to metabolic acidosis.
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