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Effect of propranolol in dinitrophenol poisoning.

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.