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首页> 外文期刊>American Journal of Physiology >Oxygen supply and oxidative phosphorylation limitation in rat myocardium in situ.
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Oxygen supply and oxidative phosphorylation limitation in rat myocardium in situ.

机译：大鼠心肌原位的供氧和氧化磷酸化限制。

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The 1H-NMR signal of the proximal histidyl-N(delta)H of deoxymyoglobin is detectable in the in situ rat myocardium and can reflect the intracellular PO2. Under basal normoxic conditions, the cellular PO2 is sufficient to saturate myoglobin (Mb). No proximal histidyl signal of Mb is detectable. On ligation of the left anterior descending coronary artery, the Mb signal at 78 parts/million (ppm) appears, along with a peak shoulder assigned to the corresponding signal of Hb. During dopamine infusion up to 80 microg. kg(-1) x min(-1), both the heart rate-pressure product (RPP) and myocardial oxygen consumption (MVO2) increase by about a factor of 2. Coronary flow increases by 84%, and O2 extraction (arteriovenous O2 difference) rises by 31%. Despite the increased respiration and work, no deoxymyoglobin signal is detected, implying that the intracellular O2 level still saturates MbO2, well above the PO2 at 50% saturation of Mb. The phosphocreatine (PCr) level decreases, however, during dopamine stimulation, and the ratio of the change in P(i) over PCr (DeltaP(i)/PCr) increases by 0.19. Infusion of either pyruvate, as the primary substrate, or dichloroacetate, a pyruvate dehydrogenase activator, abolishes the change in DeltaP(i)/PCr. Intracellular O2 supply does not limit MVO2, and the role of ADP in regulating respiration in rat myocardium in vivo remains an open question.
机译：在原位大鼠心肌中可检测到脱氧肌红蛋白的近端组织基-NH的1H-NMR信号，并可反映细胞内PO2。在基础常氧条件下，细胞PO2足以饱和肌红蛋白（Mb）。没有检测到Mb的近端组氨酸信号。结扎左冠状动脉前降支后，出现Mb信号（百万分之78），以及对应于Hb信号的峰肩。在多巴胺输注过程中，最高可达80微克。 kg（-1）x min（-1），心率-压力乘积（RPP）和心肌耗氧量（MVO2）均增加约2倍。冠状动脉血流量增加84％，O2提取（动静脉O2差异）增加了31％。尽管呼吸和工作量增加，但仍未检测到脱氧肌红蛋白信号，这表明细胞内O2水平仍会饱和MbO2，远高于POb（Mb饱和度为50％）。然而，在多巴胺刺激过程中，磷酸肌酸（PCr）含量降低，P（i）与PCr的变化之比（DeltaP（i）/ PCr）增加0.19。输注丙酮酸（作为主要底物）或输注二氯乙酸盐（一种丙酮酸脱氢酶激活剂）可以消除DeltaP（i）/ PCr的变化。细胞内的氧气供应并不限制MVO2，ADP在体内调节大鼠心肌呼吸的作用仍然是一个悬而未决的问题。

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