A Further Study of the Augmenting Action of Nictine upon the Epinephrine Secretion from the Suprarenals of the Non=Anaesthetized Dog

抄録

Influence of nicotine upon the epinephrine output rate, the mean arterial blood pressure and the blood sugar concentration were determined in the dogs, non-fastened, non-anaesthetized, without evoking pain.
Although the epinephrine output was measured by Watanabe in the dogs, in physiological conditions as normal as possible, other than nicotine poisoning, the short interval of time just after injection was regrettably omitted there, owing to difficulties of managing the animal in the intoxication period. But this time is in fact just that betraying a maximally accelerated secretion of epinephrine, judging from the experiments undertaken under narcosis.
Our expectation has been realized, the blood samples from the suprarenals, collected 30 seconds long from the moment of starting injection (1 mgrm. nicotine per kilo intravenously), showed the maximum acceleration. The absolute value was 0.01 mgrm.-0.0007 mgrm. per kilo per minute from the one gland, or several hundreds to seventy times the preinjection rate. That in the second or subsequent 30 seconds period was about two-thirds of the preceding period, then afterwards it diminished quickly, so that usually about 5-10 minutes later the epinephrine output rate was found almost similar to the pre-injection period. But this length of the hyperepinephrinaemic period is thus far longer in nonanaesthetized dogs, compared to the animals under narcosis.
The period of the great acceleration must be taken as very brusque.
The period of the largest acceleration in the epinephrine liberation corresponds to the spell where the blood pressure fell abruptly, and at the end of this first 30 seconds period the pressure set in to elevate, and in the second 30 seconds period the elevation reached its maximum.
Thus it may be comprehensible that the maximum acceleration in the epinephrine discharge occurs almost simultaneously with the blood pressure fall and precedes the pressure elevation.
The changes in the blood sugar concentration occurred more slowly than those in the arterial pressure.
The denervation of the suprarenal gland, -there the splanchnic nerves were cut-, caused some diminution in the acceleration of the epinephrine output rate if the figures obtained in one and the same dog, one gland with the intact innervation, another denervated, be compared with each other. This finding might be explained by assuming some action of nicotine on the nervous mechanism for regulating the epinephrine liberation, besides on the suprarenal medulla. But the authors will not pronounce it now because of the smallness of experience.