Bachmann E, Weber E
Swiss Federal Institute of Technology, Schwerzenbach, Switzerland.
Pharmacology. 1988;36(4):238-48. doi: 10.1159/000138390.
Oxfenicine (S-4-OH-phenyl-glycine) was proposed as a compound which would stimulate carbohydrate utilization in the heart and thus reduce oxygen requirement, especially in ischemic heart disease. Oral administration to rats for several weeks gave rise to an increase in heart, liver and kidney weights. The drug damaged mitochondrial metabolism, reducing oxygen consumption and uncoupling oxidative phosphorylation in all three organs. In heart mitochondria creatine phosphate kinase was inhibited and the creatine content of the mitochondria increased. Myocyte membrane functions (Ca uptake as well as Na/K-, Mg- and Ca-ATPases) were inhibited. In all three organs lipids (phospholipids and triglycerides) as well as free fatty acids showed a transient accumulation.
氧苯尼辛（S-4-羟基苯基甘氨酸）被认为是一种能够刺激心脏碳水化合物利用从而降低氧需求的化合物，尤其是在缺血性心脏病中。给大鼠口服该药数周会导致心脏、肝脏和肾脏重量增加。该药物损害线粒体代谢，降低所有三个器官的氧消耗并使氧化磷酸化解偶联。在心脏线粒体中，肌酸磷酸激酶受到抑制，线粒体中的肌酸含量增加。心肌细胞膜功能（钙摄取以及钠/钾-、镁-和钙-ATP酶）受到抑制。在所有三个器官中，脂质（磷脂和甘油三酯）以及游离脂肪酸都出现了短暂积累。
