Tverskaya M S, Sukhoparova V V, Karpova V V, Kadyrova M Kh, Klyuchikov V Yu
N. I. Pirogov Russian Research Medical University, Moscow, Russia.
Bull Exp Biol Med. 2013 Jan;154(3):306-8. doi: 10.1007/s10517-013-1937-3.
Metabolism of contractile cardiomyocyte in experimental pulmonary stenosis complicated or not complicated by heart failure was studied by histochemical methods. In pulmonary stenosis not complicated by heart failure, intensification of glycolysis, more intense oxidation of free fatty acids and their metabolites, and acceleration of the citric acid cycle were found in the contractile cardiomyocytes. In pulmonary stenosis complicated by heart failure, glycogen content in the myocardium was sharply decreased. The histochemical enzyme profile of contractile cardiomyocytes is similar in pulmonary stenosis with and without heart failure. Comparative analysis of changes occurring in acute increase in afterload of the left or right ventricle suggested that in the latter case, metabolic abnormalities in the contractile cardiomyocytes are relatively unimportant in the pathogenesis of heart failure.
采用组织化学方法研究了实验性肺动脉狭窄合并或未合并心力衰竭时收缩性心肌细胞的代谢情况。在未合并心力衰竭的肺动脉狭窄中，收缩性心肌细胞出现糖酵解增强、游离脂肪酸及其代谢产物氧化更强烈以及柠檬酸循环加速。在合并心力衰竭的肺动脉狭窄中，心肌糖原含量急剧下降。合并和未合并心力衰竭的肺动脉狭窄中，收缩性心肌细胞的组织化学酶谱相似。对左心室或右心室后负荷急性增加时发生的变化进行比较分析表明，在后一种情况下，收缩性心肌细胞的代谢异常在心力衰竭发病机制中相对不重要。
