CARBOHYDRATE METABOLISM AFTER BURNING
Authors: Clark E. J. , Rossiter R. J. 
Published: December 2014

1. Burning caused a rise in the blood sugar of both rats and rabbits anæsthetised with ether. In rabbits, this rise was greater in well‐fed animals than in those starved for 24 hours, and had completely disappeared 24 hours after burning. In both species, adrenaline injections produced a similar hyperglycæmia. In rats, whose adrenals had been removed, there was no rise in blood sugar after burning.

2. Rats had a higher blood lactic acid one hour, but not 3 hours, after burning; adrenaline injections produced similar changes in blood lactic acid.

3. Both one and 3 hours after burning, there was a fall in the glycogen content of the whole carcass (chiefly muscle glycogen) of rats. Similar changes were observed after adrenaline injections. The carcass glycogen of burned adrenalectomised animals remained normal.

4. Rabbits deprived of food for 24 hours and burned, had a lower liver glycogen, both 4 and 24 hours after burning, than the controls, which had been merely anæsthetised. On the other hand, burning produced no change in the liver glycogen of either normal or adrenal‐ectomised rats starved for 24 hours, but the injection of adrenaline caused a slight rise.

5. Liver slices from rabbits killed 4 hours after burning formed glycogen from glucose less readily than slices from anæsthetised control animals. Slices from similar animals, killed 2‐4 hours after an injection of adrenaline which produced a similar degree of hyperglycæmia, formed glycogen normally.

6. Liver brei from burned rabbits did not break down glycogen, either by phosphorylase or amylase activity, any more rapidly than a similar brei from control animals.

7. There was no increase in the amylase activity of serum of rabbits either 4 or 24 hours after burning.

8. There was a fall in the ascorbic acid content of the adrenal gland of rabbits, both 4 and 24 hours after burning, but no change in the ascorbic acid of the liver.

9. Injection of 5 ml. of isotonic ammonium chloride intraperitoneally into rats caused a rise in blood sugar of the same order as that observed after burning, but the plasma alkali reserve, after such an injection, was much less than that observed after burning. Intraperitoneal injection of 5 ml. of isotonic sodium bicarbonate did not influence the burn hyperglycæmia any more than a similar injection of 5 ml. isotonic sodium chloride. It is concluded that acidosis plays no part in burn hyperglycæmia.

10. Well‐fed rats were no better able to survive burning than similar animals starved for 24 hours.

11. The mechanism of burn hyperglycæmia is discussed. It is concluded that there are at least two distinct processes at work:

(a) the liberation of adrenaline from the adrenal glands;

(b) some other process or processes, either stimulating hepatic glycogenolysis or inhibiting glycogenesis.

12. The source of the glucose is chiefly the muscle glycogen, and it is suggested that it is mobilised by a mechanisnm similar to the Cori cycle.

13. As a practical measure, it is suggested that during the period of shock and hæmoconcentration burn patients should be given diets rich in carbohydrate.

The authors wish to thank Professor R. A. Peters, F.R.S., for his continued interest in this work. Thanks are due to Miss J. Jenkins for valuable technical assistance. One of us (E. J. C.) is indebted to the Medical Research Council and one (R. J. R.) to the Carnegie Trustees for a personal grant. The Medical Research Council has also contributed towards the cost of this investigation.