Kolarova R, Petkov O, Popova N
Research Medico-Biological Institute, Medical Academy, Sofia, Bulgaria.
Acta Physiol Pharmacol Bulg. 1991;17(2-3):111-7.
With a view to clarifying the mechanisms of haemodynamic stress, as well as the role of some neurotransmitter systems in the pathogenesis of myocardial hypertrophy (MH), a complex of experiments was carried out with an MH model induced in rats by isoprenaline treatment and by applying the M-cholinolytic agent atropine and the alpha-adrenergic blocker phentolamine in a part of the experimental groups. The changes in the activity of some enzymes of myocardial metabolism, namely: glucose-6-phosphate dehydrogenase, pyruvate kinase, alpha-hydroxy-butyrate dehydrogenase, isocitrate dehydrogenase, malate dehydrogenase and creatine phosphokinase, were traced in 33 male Wistar rats. Considerable activation of glucose-6-phosphate dehydrogenase was found in the different experimental groups, suggesting the adaptive "anti-stress" character of this change. The results of the pathobiochemical studies presuppose the substantial participation of the alpha-adrenergic and of the M-cholinergic systems in the stage of compensated isoprenaline-induced myocardial hypertrophy.
为了阐明血流动力学应激机制以及某些神经递质系统在心肌肥大(MH)发病机制中的作用,我们用异丙肾上腺素诱导大鼠建立MH模型,并在部分实验组中应用M胆碱能阻滞剂阿托品和α肾上腺素能阻滞剂酚妥拉明,进行了一系列实验。我们追踪了33只雄性Wistar大鼠心肌代谢中某些酶的活性变化,这些酶包括:葡萄糖-6-磷酸脱氢酶、丙酮酸激酶、α-羟丁酸脱氢酶、异柠檬酸脱氢酶、苹果酸脱氢酶和肌酸磷酸激酶。在不同实验组中均发现葡萄糖-6-磷酸脱氢酶有显著激活,表明这种变化具有适应性“抗应激”特征。病理生化研究结果表明,α肾上腺素能系统和M胆碱能系统在异丙肾上腺素诱导的代偿性心肌肥大阶段中发挥了重要作用。