Katz L A, Koretsky A P, Balaban R S
Laboratory of Cardiac Energetics, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892.
Am J Physiol. 1988 Jul;255(1 Pt 2):H185-8. doi: 10.1152/ajpheart.1988.255.1.H185.
31P-NMR studies were performed to determine the tissue phosphate and oxygen consumption effects of known maneuvers on the activation of pyruvate dehydrogenase during work jumps in the perfused rat heart. In control studies of the glucose-perfused heart, work jumps, with pacing, resulted in a 32% increase in oxygen consumption (QO2) from 1.72 +/- 0.09 to 2.29 +/- 0.12 mmol O2.h-1.g dry wt-1. During this transition no significant change in the high energy phosphates were detected. In contrast, work jumps did cause changes in the phosphates when the activation of pyruvate dehydrogenase was blocked with 2.5 micrograms of ruthenium red per milliliter or maximally stimulated with 11 mM pyruvate before the increase in work. The observed increase in QO2 and inorganic phosphate and calculated increase in ADP are consistent with these phosphates controlling mitochondrial respiration under these conditions. These results suggest that the activation of pyruvate dehydrogenase and/or other dehydrogenases may be an important step in the orchestration of work and QO2.
进行了31P-NMR研究，以确定在灌注大鼠心脏的工作跳跃过程中，已知操作对丙酮酸脱氢酶激活的组织磷酸盐和氧消耗的影响。在葡萄糖灌注心脏的对照研究中，起搏引起的工作跳跃导致氧消耗（QO2）从1.72±0.09增加到2.29±0.12 mmol O2·h-1·g干重-1，增加了32%。在此转变过程中，未检测到高能磷酸盐有显著变化。相反，当在工作增加之前用每毫升2.5微克钌红阻断丙酮酸脱氢酶的激活或用11 mM丙酮酸最大程度刺激时，工作跳跃确实会导致磷酸盐发生变化。观察到的QO2和无机磷酸盐的增加以及计算得出的ADP增加与这些磷酸盐在这些条件下控制线粒体呼吸一致。这些结果表明，丙酮酸脱氢酶和/或其他脱氢酶的激活可能是协调工作和QO2的重要步骤。
