Meniño M J, Cutrín C, Vieira R, Barrio E, Parafita M A
Department of Physiology, Faculty of Biology, University of Santiago de Compostela, Galicia, Spain.
Life Sci. 1993;52(3):PL13-8. doi: 10.1016/0024-3205(93)90226-s.
Lactic acidosis has been described in patients with liver disease. Hyperlactacidaemia results from an imbalance in lactate production versus lactate utilization. It is estimated that the liver utilizes approximately 30 percent of the total lactate produced in the body under basal conditions, primarily by gluconeogenesis. The gluconeogenesis from lactate 10 mM and lactacidaemia were determined in order to investigate the effects of CCl4+ethanol administration in liver injury and, the possible effect of colchicine in our experimental fibrosis model. The tests were determined after 15, 30 or 45 days of treatment. The results indicate that the gluconeogenesis was significantly inhibited in both CCl4+ethanol groups and CCl4+ethanol+colchicine groups. By contrast, the lactacidaemia levels were much higher in the CCl4+ethanol groups than the colchicine groups. Summarising, we have documented that hyperlactacidaemia is due to the inhibition of lactate utilization by the isolated hepatocytes in experimental cirrhosis, and that the improvement in lactacidaemia caused by colchicine is not primarily due to an increase in hepatic lactate utilization.
肝病患者中曾有乳酸酸中毒的相关描述。高乳酸血症是由乳酸生成与乳酸利用失衡所致。据估计，在基础状态下，肝脏利用体内产生的总乳酸量的约30%，主要通过糖异生作用。为研究四氯化碳加乙醇给药对肝损伤的影响以及秋水仙碱在我们的实验性纤维化模型中的可能作用，测定了乳酸生成葡萄糖的过程以及10 mM的乳酸血症情况。在治疗15、30或45天后进行测试。结果表明，四氯化碳加乙醇组和四氯化碳加乙醇加秋水仙碱组的糖异生均受到显著抑制。相比之下，四氯化碳加乙醇组的乳酸血症水平比秋水仙碱组高得多。综上所述，我们已证明高乳酸血症是由于实验性肝硬化中分离的肝细胞对乳酸利用的抑制所致，并且秋水仙碱引起的乳酸血症改善并非主要归因于肝脏乳酸利用的增加。
