Arieff A I, Kerian A
Metabolism. 1976 Mar;25(3):306-12. doi: 10.1016/0026-0495(76)90088-3.
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.
通过静脉输注β-羟基丁酸,随后持续输注碳酸氢钠,在四氧嘧啶糖尿病兔中建立了自发性乳酸酸中毒模型。在一半的动物中,动脉血乳酸/丙酮酸比值从2.5 mM/0.19 mM升至20.4 mM/0.28 mM,动脉血pH降至7.16。在发生乳酸酸中毒的动物中,血液中NAD/NADH的计算比值为1437±230,而正常值为6754±1250。动脉血氧分压和血压均正常。持续输注碳酸氢钠导致血乳酸水平升高,36%的动物出现心肺骤停。接受类似治疗的正常兔未发生乳酸酸中毒。结论是,通过输注β-羟基丁酸随后输注碳酸氢钠,可在糖尿病兔而非正常兔中产生自发性乳酸酸中毒。