Abstract
The present investigation was made with the five experiments in the previous work of Sugawara and Tada1) on the normal dog as the model. Guanidine hydrochloride was intravenously administered into five bilaterally splanchnicotomized dogs, followed by blood sugar determinations. In other five individuals operated on in the same manner, because of the death of the death of the above five, adrenaline hydrochloride solution was intravenously infused with the rate nearly similar with that of the epinephrine discharge due to guanidine in the normal dogs in the previous work, and lastly the same individuals received both drugs in just the same manner as above at the same time. The blood sugar events in 4 sets (one previous and three present) were compared with each other, and the following conclusions have evolved.
(1) Contrary to the normal dog, the bilaterally splanchnicotomized dog reacts to guanidine hydrochloride only with development of hypoglycaemia, never with hyperglycaemia. Otherwise expressed, the hyperglycaemic reaction of the dog against guanidine depends upon the integrity of the splanchnic nerves.
(2) Application of guanidine and adrenaline in combination causes in the doubly splanchnicotomized dog the blood sugar fluctuation similar in degree and duration to the algebraic sum of the fluctuations causable by giving each drug. And it was also similar, in the majority of cases, with that seen in the normal dogs, poisoned with guanidine alone. Exceptional cases might possibly be explained by other subsidiary factors, though yet unknown.
The significance of the augmentation of the epinephrine secretion due to guanidine upon the blood sugar fluctuation simultaneously occurring has been thus first elucidated in the quantitative way; in other words: If the suprarenals be rendered impossible to liberate the epinephrine guanidineinduces only along-lasting, progressive decrease of the blood sugar concentration; the blood sugar increase above this low concentration, which appears itself in the earlier stage of poisoning as the hyperglycaemia, is quantitatively due to the accelerated epinephrine liberation, simultaneously occuring.
