Hemodynamic and hepatic pH responses to sodium bicarbonate and Carbicarb during systemic acidosis

Rats subjected to ammonium chloride-induced metabolic acidosis were given alkalinization therapy with either sodium bicarbonate or Carbicarb. Ammonium chloride-induced severe metabolic acidosis had minimal effect on mean arterial blood pressure and cardiac output. This acidosis resulted in a small but statistically significant fall in intracellular liver pH (pHi) as measured with 31P magnetic resonance spectroscopy (7.01 +/- 0.05 vs 7.08 +/- 0.04, p less than 0.05). Sodium bicarbonate treatment resulted in systemic alkalinization and increases in arterial pCO2 as well as transient but extreme decreases in cardiac output and mean arterial pressure. Alkalinization with sodium bicarbonate also resulted in a transient but significant decrease in intracellular liver pH (7.02 +/- 0.06 at 5 min vs 7.09 +/- 0.06 at baseline, p less than 0.05). Carbicarb therapy resulted in systemic alkalinization without major changes in arterial pCO2, cardiac output, or mean arterial blood pressure. Moreover, Carbicarb effected a sustained intracellular alkalinization of the liver (phi = 7.12 +/- 0.07 at 5 min, p less than 0.05, pHi = 7.19 +/- 0.07 at 10 min, p less than 0.01, pHi = 7.16 +/- 0.06 at 15 min, p less than 0.01, vs baseline pHi = 7.05 +/- 0.06). These data suggest that Carbicarb may be a more effective buffer than sodium bicarbonate during conditions where ventilation is limited and hemodynamic instability is present.