Relationship Between Eosinopenic Response to Cold Application and the Adrenal Gland in the Dog

The dogs were immersed into the ice water for periods of 18-55 minutes. Following withdrawal from the ice water bath, peripheral blood was sampled at an interval of 30 minutes for 5-8 hours and was used for the eosinophil counts. Bilateral adrenalectomy was performed on dogs without anesthesia. The right adrenal gland had been extirpated about 4-20 days before and the left gland at the day of observation. Cold application induced a profound fall in the number of the circulating eosinophils of the intact and of the chronically adrenal demedullated dog, its lowest level being noted within approximately 2-4 hours after the withdrawal. However, the adrenalectomized dog exhibited no or only a slight and transient fall in the eosinophil levels following cold application. Our results seem to warrant the conclusion that the eosinopenic response of the intact dog to cold application is, in the major part, due to the increased adrenal cortical activity

Effect of Tubocurarine on the Adrenal Medulla

In experiments of suprareno-jugular anastomosis on dogs, MALME"JAc and GROSS" provided evidence that tubocurarine was capable of preventing the accelerating action of anoxia on the adrenaline secretion. In this view, the present study was attempted to investigate quantitatively how tubocurarine interferes with the adrenaline-secretory action of acetylcholine. Experiments were performed on six dogs anesthetized with Evipan-sodium, whose adrenal venous blood was collected by the lumbar route method.3 " The adrenaline content of the blood specimens was determined by the method of BLOOR & BULLRN." Intravenous injections of acetylcholine in a dose of 2 mg/kg were made twice before and after application of tubocurarine. In the first place, tubocurarine was injected into the central end of the ligated coeliac artery in a dose of 1 unit/kg. When the first injection of acetylcholine was made before tubocurarine, the rate of adrenaline secretion reached its maximal value such as 0.61-1.7 ,ug/kg/min. in the first sixty-second period after the start of injection. After tubocurarine, the rate of adrenaline secretion was also increased by the second acetylcholine injection, 0.53-1.7 peg/kg/min. being estimated there. Thus, no inhibitory effect of tubocurarine upon the augmented adrenaline secretion causable by acetylcholine was observed. In the second place, ani injection of tubocurarine was made directly into the adrenal tissue in a dose o` 4 units. On receiving acetylcholine before tubocurarine, the adrenaline secretion rate was found to be 0.99-1.3 ,ug/kg/min. After tubocurarine, the second acetylcholine injection resulted in an increase in adrenaline secretion rate, 0.31-0.78 ,ag being determined. In this case, the inhibitory effect of tubocurarine was slight and not definitive. Hereupon, in doses we have used, we failed to confirm the inhibitory effect of tubocurarine on the adrenaline-secretory action of acetylcholine