Drake A J, Papadoyannis D E, Butcher R G, Stubbs J, Noble M I
Circ Res. 1980 Sep;47(3):338-45. doi: 10.1161/01.res.47.3.338.
We measured glucose metabolism in five dogs before and 3 weeks after cardiac denervation; after this time myocardial norepinephrine is depleted. The discharge by the myocardium, of 14CO2 from infused 14C-D-glucose (U), decreased following denervation (P = 0.05). The ratio of 14CO2 to total CO2 production, which measured the proportion of glucose to total substrate oxidized, also decreased following denervation (P = 0.05). The inhibition of glucose oxidation by denervation was not due to an increase in arterial lactate concentration. There was an associated increase in myocardial content of fructose-6-phosphate in an additional seven dogs (P < 0.01). We postulate that myocardial tissue norepinephrine is one of the controllers of the activity of phosphofructokinase.
我们在五只狗心脏去神经支配前后测量了葡萄糖代谢;在此之后,心肌去甲肾上腺素会耗尽。去神经支配后,注入的14C-D-葡萄糖(U)产生的14CO2的心肌排出量减少(P = 0.05)。14CO2与总CO2产生量的比值,该比值测量了葡萄糖在氧化的总底物中所占的比例,去神经支配后也降低了(P = 0.05)。去神经支配对葡萄糖氧化的抑制并非由于动脉乳酸浓度的增加。另外七只狗的心肌中6-磷酸果糖含量也相应增加(P < 0.01)。我们推测心肌组织去甲肾上腺素是磷酸果糖激酶活性的控制因素之一。