Hörl W H, Schaefer R M, Haag M, Heidland A
Miner Electrolyte Metab. 1987;13(1):7-12.
In order to evaluate the potential role of hyperkalemia and metabolic acidosis on the disturbances of carbohydrate metabolism normally seen in uremia, a specific model of acute uremia devoid of hyperkalemia and severe metabolic acidosis was chosen. Therefore, rats were deprived of potassium prior to induction of acute uremia. Potassium depletion caused a significant decrease of muscle and liver glycogen due to activation of phosphorylase kinase, whereas glycogen concentration in heart muscle was unchanged and elevated in the kidney of sham-operated and ureter-ligated animals. In contrast, glucose concentrations were enhanced in the liver and the kidney, unchanged in heart muscle and decreased in skeletal muscle. We conclude that carbohydrate abnormalities occur in acute uremia despite normokalemia and mild metabolic acidosis. Furthermore, acute uremia accompanied by prior potassium depletion results in no net effect on cardiac glycogen metabolism but stimulates glycogenolysis in both skeletal muscle and the liver.
为了评估高钾血症和代谢性酸中毒在尿毒症中常见的碳水化合物代谢紊乱中的潜在作用，我们选择了一种无高钾血症和严重代谢性酸中毒的急性尿毒症特定模型。因此，在诱导急性尿毒症之前，大鼠被剥夺了钾。钾缺乏由于磷酸化酶激酶的激活导致肌肉和肝脏糖原显著减少，而假手术和输尿管结扎动物的心肌糖原浓度未改变且肾脏中升高。相反，肝脏和肾脏中的葡萄糖浓度升高，心肌中未改变，骨骼肌中降低。我们得出结论，尽管血钾正常和轻度代谢性酸中毒，急性尿毒症中仍会出现碳水化合物异常。此外，伴有先前钾缺乏的急性尿毒症对心脏糖原代谢没有净影响，但会刺激骨骼肌和肝脏中的糖原分解。
