Markov A K, Oglethorpe N C, Blake T M, Lehan P H, Hellems H K
Am Heart J. 1980 Nov;100(5):639-46. doi: 10.1016/0002-8703(80)90228-8.
The hemodynamic, electrocardiographic, and metabolic responses of dogs with acute myocardial ischemia to intravenous administration of fructose-1,6-diphosphate (FDP) were assessed. Analysis of the results (compared to dextrose control) revealed evidence of major improvement of LVEDP and cardiac output, significant decrease of the ST segment, and large increases of ATP and CP in the ischemic district and to a lesser degree in the normally perfused myocardium. These results indicate that FDP intervenes in the Embden-Meyerhof pathway not only as a high energy substrate but also as a metabolic regulator influencing the activity of phosphofructokinase and that of pyruvate kinase. FDP also stimulates glycolysis in dog erythrocytes and increases their ATP and 2-3 DPG content by a factor of 2. The most significant finding in these studies is that this biochemical intervention appears to restore the depressed activity of glycolysis in ischemic myocardium.
评估了急性心肌缺血犬静脉注射1,6 -二磷酸果糖(FDP)后的血流动力学、心电图和代谢反应。对结果的分析(与葡萄糖对照相比)显示,左心室舒张末期压力(LVEDP)和心输出量有显著改善,ST段明显下降,缺血区的三磷酸腺苷(ATP)和磷酸肌酸(CP)大幅增加,在正常灌注心肌中增加程度较小。这些结果表明,FDP不仅作为一种高能底物参与糖酵解途径,还作为一种代谢调节剂影响磷酸果糖激酶和丙酮酸激酶的活性。FDP还刺激犬红细胞的糖酵解,并使其ATP和2,3 -二磷酸甘油酸(2,3 - DPG)含量增加两倍。这些研究中最显著的发现是,这种生化干预似乎恢复了缺血心肌中受抑制的糖酵解活性。