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.
D019297:2,4-Dinitrophenol; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D001831:Body Temperature / Q000187:drug effects; D004140:Dinitrophenols / Q000506:poisoning*; D004285:Dogs; D007700:Kinetics; D007773:Lactates / Q000378:metabolism*; D019344:Lactic Acid; D008099:Liver / Q000378:metabolism; D010710:Phosphates / Q000378:metabolism; D011433:Propranolol / Q000494:pharmacology*
D001786:Blood Glucose; D004140:Dinitrophenols; D007773:Lactates; D010710:Phosphates; D019344:Lactic Acid; D011433:Propranolol; D019297:2,4-Dinitrophenol