Weiss J, Hiltbrand B
J Clin Invest. 1985 Feb;75(2):436-47. doi: 10.1172/JCI111718.
To investigate whether energy derived from glycolytic and oxidative metabolism are preferentially used for different functions in heart, tension, intracellular potential, and extracellular [K+] and pH (using triple barrel K/pH electrodes, tip diameter 0.5 mm) were monitored in isolated arterially perfused rabbit interventricular septa during exposure to hypoxia and metabolic inhibitors. Myocardial content of high energy phosphates, lactate, and glycogen were determined under the same conditions. Inhibiting oxidative metabolism with hypoxia, dinitrophenol (10(-5)M), or Na-azide (10(-3)M) caused marked suppression of tension (by 73 +/- 5, 65 +/- 8, and 50 +/- 14%, respectively) and a small increase in [K+]0 (0.8 +/- 0.4, 0.5 +/- 0.25, and 0.4 +/- 0.2 mM, respectively) after 10 min. Inhibiting glycolysis with iodoacetate (IAA) (10(-3)M) had a much smaller suppressant effect on tension (28 +/- 24%) but markedly increased [K+]0 accumulation (by 1.8 +/- 1.1 mM) at 10 min. These differences, when IAA was compared individually to the other interventions, were highly significant. The shortening of action potential duration was not significantly different for the four interventions. pH0 increased slightly during IAA (+0.04-+0.06 U) and fell during the other interventions (-0.10--0.16 U), but this did not account for the differences in [K+]0 accumulation and tension between inhibition of glycolytic vs. oxidative metabolism. Except for hypoxia, total cellular content of high energy phosphates was not significantly depressed under the various conditions. This data suggests that energy from glycolysis is preferentially used to support sarcolemmal function (as manifested by K+ loss), whereas oxidatively derived energy preferentially supports contractile function. Indexing terms: cardiac metabolism, extracellular pH, metabolic inhibitors, hypoxia, extracellular K+ accumulation, and glycolysis.
为研究源自糖酵解代谢和氧化代谢的能量是否优先用于心脏的不同功能，在暴露于缺氧和代谢抑制剂的情况下，对离体动脉灌注兔室间隔的张力、细胞内电位以及细胞外[K⁺]和pH（使用三管K/pH电极，尖端直径0.5毫米）进行监测。在相同条件下测定高能磷酸盐、乳酸和糖原的心肌含量。用缺氧、二硝基苯酚（10⁻⁵M）或叠氮化钠（10⁻³M）抑制氧化代谢，10分钟后可导致张力显著抑制（分别为73±5%、65±8%和50±14%）以及[K⁺]₀小幅升高（分别为0.8±0.4、0.5±0.25和0.4±0.2 mM）。用碘乙酸（IAA）（10⁻³M）抑制糖酵解对张力的抑制作用小得多（28±24%），但在10分钟时显著增加[K⁺]₀积累（增加1.8±1.1 mM）。当将IAA与其他干预措施单独比较时，这些差异非常显著。四种干预措施使动作电位持续时间缩短的情况无显著差异。在IAA作用期间pH₀略有升高（+0.04 - +0.06单位），在其他干预措施作用期间下降（-0.10 - -0.16单位），但这并不能解释糖酵解与氧化代谢抑制之间[K⁺]₀积累和张力的差异。除缺氧外，在各种条件下高能磷酸盐的总细胞含量无显著降低。这些数据表明，糖酵解产生的能量优先用于支持肌膜功能（表现为K⁺丢失），而氧化产生的能量优先支持收缩功能。索引词：心脏代谢、细胞外pH、代谢抑制剂、缺氧、细胞外K⁺积累和糖酵解。
