Otorii T, Katano Y, Takeda K, Imai S
Jpn Heart J. 1980 Nov;21(6):845-57. doi: 10.1536/ihj.21.845.
Piridoxilate is a conjugation product of pyridoxine and glyoxylic acid, which may be a physiological regulator of cell respiration. Effects of this substance on the oxidation-reduction state of the pyridine nucleotides in the heart were studied using the canine heart-lung preparation supported by a donor dog. The oxidation-reduction state of the heart was estimated using the following 2 parameters: 1) myocardial redox potential and 2) NADH fluorescence in the heart muscle. In doses above 0.4 mM, piridoxilate produced a marked shift to more positive values of the myocardial redox potential and a decrease in NADH fluorescence. In contrast, ventilation of the animal with N2 gas and infusion of NaCN into the preparation resulted in a shift to more negative values of myocardial redox potential and an increase in NADH fluoresecence of the heart muscle. After pretreatment of the preparation with piridoxilate, the depression of redox potential and the increase in NADH fluorescence produced by N2 gas inhalation or by NaCN infusion were clearly reduced. These findings suggest a protective action of piridoxilate against hypoxia which may be attributable to rearrangement of the myocardial metabolism.
吡哆醛酸是吡哆醇和乙醛酸的结合产物，可能是细胞呼吸的一种生理调节剂。使用由供血犬支持的犬心肺制备模型，研究了该物质对心脏中吡啶核苷酸氧化还原状态的影响。心脏的氧化还原状态通过以下两个参数进行评估：1）心肌氧化还原电位和2）心肌中的NADH荧光。当剂量高于0.4 mM时，吡哆醛酸会使心肌氧化还原电位显著向更正的值偏移，并使NADH荧光降低。相反，用N2气体对动物进行通气并向制备模型中注入NaCN会导致心肌氧化还原电位向更负的值偏移，且心肌的NADH荧光增加。在用吡哆醛酸对制备模型进行预处理后，由吸入N2气体或注入NaCN所导致的氧化还原电位降低和NADH荧光增加明显减轻。这些发现表明吡哆醛酸对缺氧具有保护作用，这可能归因于心肌代谢的重新调整。
