p1. The contribution of Co2 fixation to the anaplerotic mechanisms in the myocardium was investigated in isolated perfused rat hearts. 2. K+-induced arrest of the heart was used to elicit a transition in the concentrations of the intermediates of the tricarboxylic acid cycle. 3. Incorporation of 14C from [14]bicarbonate into tricarboxylic acid-cycle intermediates was measured and the rates of the reactions of the cycle were estimated by means of a linear optimization program which solves the differential equations describing a simulation model of the tricarboxylic acid cycle and related reactions. 4. The results showed that the rate of CO2 fixation is dependent on the metabolic state of the myocardium. Upon a sudden diminution of cellular ATP consumption, the pool size of the tricarboxylic acid-cycle metabolites increased and the rate of label incorporation from [14C]bicarbonate into the cycle metabolites increased simultaneously. The computer model was necessary to separate the rapid equilibration between bicarbonate and some metabolites from the potentially anaplerotic reactions. The main route of anaplerosis during metabolite accumulation was through malate + oxaloacetate. Under steady-state conditions there was a constant net outward flow from the tricarboxylic acid cycle via the malate + oxaloacetate pool, with a concomitant anaplerotic flow from metabolites forming succinyl-CoA (3-carboxypropionyl-CoA)./p
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机译：> 1。研究分离灌注大鼠心脏研究了CO2固定对心肌中的缠绕机制的贡献。 2. K +诱导心脏的逮捕用于引发三羧酸循环中间体的浓度的过渡。 3.测量从[14]碳酸氢盐中的14℃掺入三羧酸循环中间体，并通过线性优化程序估计循环反应的速率，该方法求解描述三羧酸周期的模拟模型的微分方程和相关的反应。结果表明，二氧化碳固定率取决于心肌的代谢状态。在突然减少细胞ATP消耗后，三羧酸循环代谢物的池尺寸增加，并且从[14C]碳酸氢盐中的标签掺入到循环代谢物中的标签掺入同时增加。需要计算机模型以将碳酸氢盐和一些代谢物之间的快速平衡分离出来自潜在的包层的反应。代谢物积累期间的厌氧过程的主要途径是通过苹果酸+草酸酯。在稳态条件下，通过苹果酸+草丙酸盐池从三羧酸循环中恒定的净向外流，来自代谢物形成琥珀酰库（3-羧基丙酰基-CoA）的代谢物的伴随的肛门粥样硬化。
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