Abstract
On the base of the experimental evidence of Sato and Ohmi of the whole figure of the oversecretion of the epinephrine output from the suprarenals in the dog by poisoning with morphine, the present writer tried to make clear the share of the oversection of epinephrine in the production of hyperglycaemia occurring simultaneously during the morphine intoxication.
Four sets of experiments were carried out: Morphine into the dogs with the intact suprarenals, morphine into the dogs with the demedullated suprarenals, adrenaline hydrochloride into the dogs so operated on and morphine and adrenaline hydrochloride into the dogs without the suprarenal medulla. Morphine hydrochloride was intravenously injected in the constant dose of 8 mgrms. per kilo of body weight, and adrenaline hydrochloride saline solution was intravenously injected with a constant velocity of 1 c. c. a minute, but its content of the drug was arranged to imitate as faithfully as possible the rate of epinephrine discharge from the suprarenal glands in the dog of Sato and Ohmi, which was injected with that dose. In some dogs all the sets of experiments were carried out, but in others the latter three sets only. The first set of experiments was performed in some other individuals.
The outstanding figures in the outcome are as follows.
(1) The whole figure of the hyperglycaemia, caused by morphine in the normal dogs and of that by morphine plus adrenaline in the dogs with the demedullated suprarenals are almost wholly identical. Morphine alone brought about the hyperglycaemia in the dogs with the demedullated suprarenals, but its figure is different in certain points from those above related to. It is clearly inferior in relation to the magnitude of them, and although the steepness of the as-cending limb is similar to them, it turns relatively early into the slow descending limb without plateau or with a short one. The continuous infusion of adrenaline-saline fluid caused hyperglycaemia definitely inferior in magnitude to those in the normal dogs under morphine, and to those in cases where the suprarenal medulla was already previously deprived of and morphine was injected in addition to the adrenaline infusion, yet it was rather similar in the form to them.
It can be stated therefore that the hyperglycaemia elicitable by morphine has two origins; one due to the oversecretion of epinephrine from the suprarenal glands, and another which has no relation to the suprarenal medulla, and probably the former has some such share therein.
(2) Of the fluctuation in the pulse rate during the morphine poisoning, the oversecretion of epinephrine from the suprarenals or the adrenaline infusion was found, though not so striking, as having some significance, and in fact a paradoxical one; that is they act rather to retard the pulse rate. This is strange enough, but has some analogy in the role of the epinephrine oversecretion in the blood sugar fluctuation during the peptone poisoning, which was elucitated by Kaiwa.
(3) The oversecretion of epinephrine during the morphine poi-soning may be taken as to effecting, though not so decidedly, to lesson the body temperature fall therein.
