Fuchs J, Zimmer G, Bereiter-Hahn J
Gustav-Embden-Zentrum der Biologischen Chemie, Universität Frankfurt, German Federal Republic.
Cell Biochem Funct. 1987 Oct;5(4):245-53. doi: 10.1002/cbf.290050403.
In perfused rat hearts alterations of aortic flow and mitochondrial membrane potential resulting from uncoupling of oxidative phosphorylation, hypoxia and treatment with a cardioprotective drug (2-mercaptopropionylglycine (MPG) have been studied. Mitochondrial membrane potential was followed by surface fluorimetry on DASPMI stained hearts. This fluorochrome specifically stains mitochondria in living cells; fluorescence intensity is related to the electrochemical gradient. Aortic flow turned out to be a much more sensitive indicator of heart function than ventricular pressure or mitochondrial membrane potential. No direct relationship exists between mitochondrial membrane potential and ATP production under the different metabolic conditions. Two phases of hypoxic mitochondrial damage have been deduced: the first results in derangement of ATP synthases while membrane potential is maintained, the second in irreversible damage of mitochondrial membranes with loss of membrane potential.
在灌注大鼠心脏中，研究了由氧化磷酸化解偶联、缺氧以及用心脏保护药物（2-巯基丙酰甘氨酸，MPG）处理所导致的主动脉血流和线粒体膜电位的变化。通过对用达普米（DASPMI）染色的心脏进行表面荧光测定来跟踪线粒体膜电位。这种荧光染料能特异性地对活细胞中的线粒体进行染色；荧光强度与电化学梯度相关。结果表明，主动脉血流是比心室压力或线粒体膜电位更敏感的心脏功能指标。在不同代谢条件下，线粒体膜电位与ATP生成之间不存在直接关系。已推断出缺氧性线粒体损伤的两个阶段：第一阶段导致ATP合酶紊乱，而膜电位得以维持，第二阶段导致线粒体膜的不可逆损伤，膜电位丧失。
