Abstract
In a study of the hyperglycemia produced by 2–4 dinitrophenol (DNP), Hall, Brown and Sahyun 1 suggested that its mechanism might be the stimulation of sympathetic glycogenolytic centers of the brain stem by local cellular anoxemia or acidosis. Wishnovsky, Kane, Schlevin and Byron 2 have criticized this suggestion, on the grounds that the rise in blood sugar produced by the drug may still be demonstrated after the administration of large quantities of glucose, at a time when, as they state “the tissues are flooded with dextrose and the predominant process in the liver is glycogenesis. There is no need for active glycogenolysis.” They were at a loss to explain the observed rise.
In order to determine whether DNP hyperglycemia depends upon impulses arising in the central nervous system and causing hepatic glycogenolysis, we have cut the 3 splanchnic nerves of cats just below the diaphragm on both sides under aseptic conditions. Controls were subjected to the same procedure except that the nerves were not actually cut. After a recovery period of at least 2 weeks, the animals were anesthetized with pentobarbital (37.5 mg. per kg. intraperitoneally), allowed to rest 90 minutes so that the hyperglycemia resulting from the excitement of anesthetization might pass off, a control blood sample drawn by heart puncture and a dose of sodium 2–4 dinitrophenolate solution, adequate to yield 10 mg. per kg. of the acid was injected intramuscularly. Blood samples were drawn 30, 60 and 120 minutes after injection, and the glucose content determined by the method of Folin and Wu. 3
The results, which appear in Table I, show that, in the controls, DNP at least doubled the blood glucose concentration, the peak usually being reached about 30 minutes after injection.
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