S. Kuriyama 2h 
From this table it will be seen that in normal rabbits epinephrine 
injection does not cause any noteworthy decrease of the CO, 
capacity of the plasma. Judging from the glycosuria and hy- 
perglycemia, the drug employed was very effective. The sugar 
estimation in one case and my previous experiments! concerning 
the epinephrine hyperglycemia show that the maximal point of 
the epinephrine hyperglycemia is usually obtained from 2 to 4 
hours after the subcutaneous injection of epinephrine. No 
marked decrease of the alkali reserve was observed even at this 
point. So far as shown by these experiments, no evidence was 
cbtained that hypersecretion of the adrenals plays any réle in 
acidosis found in thyroid-fed animals. 
The Influence of Sodium Bicarbonate upon the Decrease of the Liver 
Glycogen of Thyroid-Fed Rats. 
Pavy and Bywaters" reported that the postmortem production of 
sugar in the liver may be virtually checked by the injection of a 2 per 
cent solution of sodium carbonate into the portal system of the living 
animal. A similar effect of alkali upon the sugar production of the liver 
was reported by Pavy and Godden” in chloroform glycosuria, which is 
dependent upon the glycogen supply of the liver. A cat was made-glyco- 
suric by chloroform anesthesia, and then sodium carbonate, in 3 per cent 
solution, to the amount of 0.75 gm. per kilo of body weight, was injected 
into the femoral vein. This brought about a speedy reduction in the 
glycosuria. Murlin and Kramer!® reported that in pancreatic diabetes, 
sodium carbonate decreases glycosuria and that glucose thus retained is 
not held back as glycogen. According to them, sodium bicarbonate had 
not the same effect as sodium carbonate. Underhill,17 however, observed 
a very favorable effect of sodium bicarbonate in decreasing glycosuria in 
diabetic patients. Feeding normal rabbits on either base-forming diet (car- 
rot) or acid-forming diet (grain), McDanell and Underhill!® reported that 
the former is somewhat more efficient in the formation of liver glycogen than 
the latter. 
In connection with the rapid decrease of the liver glycogen 
and an onset of acidosis in the thyroid-fed animals, I have made 
13 Kuriyama, S., J. Biol. Chem., 1917, xxix, 127. 
14 Pavy, F. W., and Bywaters, H. W., J. Physiol., 1910-11, xli, 168. 
15 Pavy, F. W., and Godden, W., J. Physiol., 1911-12, xliii, p. vii. 
16 Murlin, J. R., and Kramer, B., J. Biol. Chem., 1916, xxvii, 481. 
Kramer, B., Marker, J., and Murlin, J. R., ibid., 1916, xxvii, 499. 
17 Underhill, F. P., J. Am. Med. Assn., 1917, Ixviii, 497. 
18 McDanell and Underhill, J. Biol. Chem., 1917, xxix, 255, 
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THE JOURNAL OF BIOLOGICAL CHEMISTRY, VOL. XXXIII, NO. 1 
