Issekutz B
Arch Int Pharmacodyn Ther. 1984 Dec;272(2):310-9.
The effect of the beta-blocker propranolol (PR) in sublethal poisoning with 2, 4,-dinitrophenol (DNP) was studied on carbohydrate kinetics in dogs. Parameters of glucose and lactate turnovers were measured by using a mixture of 3-3H-glucose and 14C-lactate according to the primed constant rate infusion technics. Participation of plasma glucose in lactate production (% L----G) and the rate of peripheral glycogenolysis (GLY) was estimated in experiments using a mixture of 3-3H-glucose and 14C-glucose (U). PR did not interfere with the DNP-induced rise of body temperature (+ 4 degrees C), but completely blocked the rise of lactate production, the lactacidemia and the rise of GLY seen in DNP treated controls. PR significantly increased %L----G, prolonged the DNP induced hyperphosphataemia and it caused a decline of plasma glucose. The effects of the beta-blocker could be overcome by increasing the rate of DNP infusion. It is concluded that in DNP poisoning the beta-adrenergic system plays a major role in the elevated peripheral glycogenolysis and it helps to compensate for the loss of mitochondrial synthesis of ATP by greatly accelerating its cytoplasmic synthesis.
研究了β受体阻滞剂普萘洛尔（PR）对狗2,4-二硝基苯酚（DNP）亚致死性中毒时碳水化合物动力学的影响。根据预充恒速输注技术，使用3-³H-葡萄糖和¹⁴C-乳酸的混合物测量葡萄糖和乳酸周转参数。在使用3-³H-葡萄糖和¹⁴C-葡萄糖（U）的实验中，估计血浆葡萄糖在乳酸生成中的参与度（%L→G）和外周糖原分解速率（GLY）。PR不干扰DNP引起的体温升高（+4℃），但完全阻断了乳酸生成增加、乳酸性血症以及DNP处理对照组中观察到的GLY升高。PR显著增加%L→G，延长DNP诱导的高磷血症，并导致血浆葡萄糖下降。增加DNP输注速率可克服β受体阻滞剂的作用。得出结论，在DNP中毒中，β肾上腺素能系统在外周糖原分解增加中起主要作用，并通过极大地加速其细胞质合成来帮助补偿线粒体ATP合成的损失。
