Effects of bicarbonate on arterial and brain intracellular pH in neonatal rabbits recovering from hypoxic lactic acidosis.
We used 31P spectroscopy to determine whether administration of a neutralizing dose of bicarbonate in rabbits with lactic acidosis caused a paradoxical brain intracellular acidosis. Ten 10- to 16-day-old rabbits were anesthetized with 0.75% halothane/oxygen and their lungs mechanically ventilated. Metabolic acidosis was induced by decreasing PaO2 to 25 to 35 mm Hg for 1 to 2 hours until the base deficit was 10 to 15 mEq/L. Cerebral ischemia was prevented by maintaining arterial blood pressure at +/- 20% of control value with a venous infusion of epinephrine. Hypoxia was then terminated by administration of 100% oxygen, which was continued for the remainder of the study. After 15 minutes 100% oxygen, 5 mEq/kg 4.2% bicarbonate was administered to five animals; 5 minutes later the same dose was repeated. Control rabbits were given equal volumes of saline solution. In all animals, arterial pH decreased from 7.43 +/- 0.06 to 7.25 +/- 0.08 (SE) during hypoxia, and brain intracellular pH from 7.22 +/- 0.06 to 7.09 +/- 0.09 (SE). Both pH values remained low during reoxygenation. Bicarbonate administration normalized arterial pH (7.41 +/- 0.03), whereas treatment with saline solution did not (7.23 +/- 0.01, P less than 0.05). PaCO2 rapidly increased by 10 mm Hg in the bicarbonate group, and remained elevated; it was unaffected by saline solution administration. Brain intracellular pH in the bicarbonate group increased by 0.12 U over 40 minutes, but intracellular pH in the saline solution group decreased 0.05 pH U (P less than 0.05) over the same period. We conclude that administering a total dose of 10 mEq/kg sodium bicarbonate to neonatal rabbits recovering from hypoxic lactic acidosis increases arterial pH, brain intracellular pH, and PaCO2; it does not produce paradoxical intracellular acidosis in the brain.
Sessler
D
D
Department of Anesthesia, University of California, San Francisco 94143-0648.
Mills
P
P
Gregory
G
G
Litt
L
L
James
T
T
D000140:Acidosis, Lactic / Q000097:blood / Q000188:drug therapy* / Q000209:etiology; D000818:Animals; D001639:Bicarbonates / Q000009:adverse effects* / Q000627:therapeutic use; D001921:Brain / Q000187:drug effects* / Q000473:pathology; D002245:Carbon Dioxide; D006863:Hydrogen-Ion Concentration; D000860:Hypoxia / Q000150:complications*; D009682:Magnetic Resonance Spectroscopy; D010313:Partial Pressure; D011817:Rabbits; D012964:Sodium / Q000009:adverse effects* / Q000627:therapeutic use; D017693:Sodium Bicarbonate
D001639:Bicarbonates; D002245:Carbon Dioxide; D017693:Sodium Bicarbonate; D012964:Sodium