Serum
lactic acidosis is characterized by a pH less than 7.25 and
lactate greater than 5 mEq. Although
sodium bicarbonate (NaHCO3) is standard treatment for this condition, clinical and experimental studies suggest that high doses of NaHCO3 may be ineffectual or even detrimental to brain, cardiovascular, and respiratory function, as well as survival. For this reason, low dose
therapy with NaHCO3 has been recommended.
Sodium dichloroacetate (NaDCA) has been used successfully to treat clinical and experimentally-induced
lactic acidosis. The present study was designed to compare the effects of low dose NaHCO3 with NaDCA on blood pressure, blood chemistries and brain metabolites in rats with a low flow-induced (Type A, the most common type)
lactic acidosis. Fasted male Wistar rats were subjected to
cerebral ischemia and systemic
hypotension for 30 min at which time, if the pH or HCO-3 fell to 7.2 or 10, respectively, the rat was treated with NaHCO3, NaDCA, or an equal volume of sterile water. Over the 30 min of recirculation that followed
ischemia, treatment had no effect on blood pressure or
glucose or on brain
glucose or
glycogen. NaHCO3 had no effect on
lactate but appeared to stabilize pH and increase HCO3- more than in
sham- or NaDCA-treated rats. Although NaDCA caused a greater increase in HCO3- than
sham treatment, pH continued to decline. However,
lactate decreased more in NaDCA- than in
sham- or NaHCO3- treated rats. These results suggest that low dose NaHCO3 is not detrimental in this model; however, although NaHCO3 stabilized pH, it did not rapidly correct the
acidosis. NaDCA at this dose had no effect on the
acidosis but was effective in decreasing
lactate. Since serum
lactate has previously correlated with survival and since higher doses of NaDCA have corrected
lactic acidosis in other studies, future evaluation of postischemic treatment with higher doses of NaDCA is warranted.