Lactic acidosis: an experimental model.
A model of spontaneous lactic acidosis was developed in alloxan diabetic rabbits by infusing intravenously beta-hydroxybutyric acid followed by a continuous infusion of NaHCO3. In half of the animals, the arterial lactate/pyruvate ratio rose from 2.5 mM/0.19mM to 20.4 mM/0.28 mM, and arterial pH fell to 7.16. In animals with lactic acidosis, the calculated ratio in blood of NAD/NADH was 1437 +/- 230, versus a normal value of 6754 +/- 1250. Both arterial PO2 and blood pressure were normal. Continued infusion of NaHCO3 led to increased blood lactate levels, with cardiorespiratory arrest in 36% of animals. Lactic acidosis did not develop in normal rabbits who were similarly treated. It is concluded that spontaneous lactic acidosis can be produced in diabetic, but not in normal, rabbits by infusion of beta-hydroxybutric acid followed by infusion of NaHCO3.
Lactic acidosis: an experimental model. A model of spontaneous lactic acidosis was developed in alloxan diabetic rabbits by infusing intravenously beta-hydroxybutyric acid followed by a continuous infusion of NaHCO3. In half of the animals, the arterial lactate/pyruvate ratio rose from 2.5 mM/0.19mM to 20.4 mM/0.28 mM, and arterial pH fell to 7.16. In animals with lactic acidosis, the calculated ratio in blood of NAD/NADH was 1437 +/- 230, versus a normal value of 6754 +/- 1250. Both arterial PO2 and blood pressure were normal. Continued infusion of NaHCO3 led to increased blood lactate levels, with cardiorespiratory arrest in 36% of animals. Lactic acidosis did not develop in normal rabbits who were similarly treated. It is concluded that spontaneous lactic acidosis can be produced in diabetic, but not in normal, rabbits by infusion of beta-hydroxybutric acid followed by infusion of NaHCO3.