Kuz'min A I, Saprygina T V, Sulimov V A, Kukes V G, Makolkin V I
Kardiologiia. 1984 Dec;24(12):55-62.
The authors revealed that concentrations of inosin, hypoxanthine and their total levels in the arterial blood and the blood of the coronary sinus in patients with paroxysmal tachycardias are higher than the corresponding levels in patients with chronic forms of coronary heart disease and neurocirculatory dystonia. In the absence of tachycardia, there was an accelerated metabolism of adenyl nucleotides of the myocardium: the myocardium produced inosin and extracted hypoxanthine. It is suggested that this type of metabolism of adenyl nucleotides requires additional energy expenditures as compared with the energy supply of the nucleotide metabolism of the healthy myocardium and may be one of the reasons underlying the development of tachycardiac paroxysm, with the place of the localization of the re-entry and/or the presence of coronary heart disease having no significant effect on the metabolism of adenyl nucleotides of the myocardium in such patients. The emergence of tachycardia leads to a decreased extraction of hypoxanthine by the myocardium as compared to the baseline and to insignificant elevation in the production of inosin which causes an increase in the levels of these metabolites in the arterial blood and the blood of the coronary sinus.
作者发现,阵发性心动过速患者动脉血和冠状窦血液中肌苷、次黄嘌呤的浓度及其总水平高于慢性冠心病和神经循环性肌张力障碍患者的相应水平。在无心动过速的情况下,心肌腺苷酸代谢加速:心肌产生肌苷并摄取次黄嘌呤。提示这种腺苷酸代谢类型与健康心肌核苷酸代谢的能量供应相比需要额外的能量消耗,可能是心动过速发作的原因之一,折返定位部位和/或冠心病的存在对此类患者心肌腺苷酸代谢无显著影响。与基线相比,心动过速的出现导致心肌对次黄嘌呤的摄取减少,肌苷生成略有升高,从而导致这些代谢产物在动脉血和冠状窦血液中的水平升高。