Ivanov A I, Khitrov N K
Kardiologiia. 1983 Jan;23(1):94-8.
Energy deficiency caused by 2,4-dinitrophenol (2,4-DNP), stimulates cardiac activity, increases noradrenaline (NA) content in the heart, but decreases the latter's adrenoreactivity. The removal of stellate ganglia reduces myocardial hyperfunction and prevents the rise of the cardiac NA content. Increasing the dose of 2,4-DNP inhibits cardiac activity and reduces cardiac NA and myocardial adrenoreactivity. Prolonged 2,4-DNP administration increases resistance to hypoxia in rats. Ten-day exposure to 2,4-DNP enhances the stability of the cardiac NA level and myocardial adrenoreactivity. By day 20, the reserve potential of myocardial contractility is enhanced, but the adaptive changes in the myocardial neuronic apparatus disappear. When circulation is stimulated, adaptive changes in sympathetic neurons and the myocardium develop and disappear after a certain pattern under the effect of energy deficiency.
2,4-二硝基苯酚（2,4-DNP）引起的能量缺乏会刺激心脏活动，增加心脏中去甲肾上腺素（NA）的含量，但会降低后者的肾上腺反应性。切除星状神经节可减轻心肌功能亢进，并防止心脏NA含量升高。增加2,4-DNP的剂量会抑制心脏活动，并降低心脏NA和心肌肾上腺反应性。长期给予2,4-DNP可增加大鼠对缺氧的抵抗力。暴露于2,4-DNP十天可增强心脏NA水平和心肌肾上腺反应性的稳定性。到第20天时，心肌收缩力的储备潜力增强，但心肌神经装置的适应性变化消失。当循环受到刺激时，在能量缺乏的作用下，交感神经元和心肌的适应性变化会按一定模式发展并消失。
