Studies on alterations of free aromatic amino acids and protein turnover in skeletal muscles under surgical stresses.

我们研究了无肝功能障碍的创伤或感染患者中经常观察到的血苯丙氨酸浓度升高与经历病理生理学不同应激（脓毒症或肝损伤）的大鼠中肝苯丙氨酸催化剂改变之间的关系。磷酸肌酸的分解维持了腹肌、股肌和膈肌组织中腺嘌呤核苷酸水平和能量状态，但促进了这些组织中蛋白质的降解。在这些应力下，腹肌和股肌中许多氨基酸水平的变化超过了血浆中相应氨基酸水平的变化。观察到的血浆和肌肉中游离氨基酸的变化很好地反映了骨骼肌中蛋白质降解的增强。苯丙氨酸羟化酶的活性，使用天然存在的辅因子测量，下降了40%，而苯丙氨酸丙酮酸氨基转移酶被激活的25%，与对照组相比，在脓毒症大鼠的肝脏。这种激活，由胰高血糖素水平的增加引起，导致苯丙氨酸的氧化比对照组增加76%，如通过脉冲施用13 <14>C-标记的苯丙氨酸所测量的。在烫伤大鼠血浆苯丙氨酸水平表现出可比的，但暂时上升，这些酶的活性和苯丙氨酸氧化没有发生显着变化。这些结果表明，苯丙氨酸羟基化的减少也是负责感染大鼠的血浆苯丙氨酸水平的升高，在大量动员的氨基酸从骨骼肌的条件下，增强和持续catalysts。

We examined the relationship between the elevation of blood phenylalanine concentrations often observed In trauma or infected patients without hepatic dysfunction and alterations of liver phenylalanine catabolism in rats undergoing pathophysiologically different stresses, either sepsis or scald injury. The adenine nucleotide levels and the energy state in tissues of abodominal and femoral muscles and diaphragm were maintained by breakdown of phosphocreatine, but protein degradation was promoted in these tissues. The alterations of many amino acid levels in abdominal and femoral muscles paralleled those of the corresponding amino acid levels in plasma under these stresses. The observed changes in free amino acids in plasma and the muscles well reflected the enhanced protein degradation in skeletal muscles. Phenylalanine hydroxylase activity, as measured using a naturally occurring cofactor, decreased by 40%, while phenylalanine-pyruvate aminotransferase was activated by 25% in the livers of the septic rats as compared with those of the controls. Such activation, caused by an increase in glucagon levels, resulted in a 76% increase in oxidation of phenylalanine over that of controls, as measured by pulse-administration of ^<14>C-labeled phenylalanine. In the scalded rats whose plasma phenylalanine level showed a comparable but temporary rise, no significant alterations in these enzyme activities and phenylalanine oxidation occurred. These results indicate that reduction of phenylalanine hydroxylation was also responsible for the elevation of the plasma phenylalanine level in infected rats during massive mobilization of amino acids from skeletal muscles under conditions of enhanced and sustaining catabolism.