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Normal, pantothenic acid-deficient and riboflavin-deficient young dogs were forced to swim for 25 minutes at 25°C and their blood glucose and in some cases blood lactic acid levels determined just before, just after and 1 and 2 hours after the test. A sharp rise in blood sugar level, markedly greater in the riboflavin-deficient dogs, occurred just after the swimming stress. An abnormal fall in level occurred in all deficient dogs after 2 hours. Severe under-feeding did not produce this change in a normal dog nor did force feeding alter it in riboflavin-deficient animals. Adrenocortical extract treatment diminished the poststress rise in normal and pantothenic acid-deficient but not in riboflavin-deficient dogs. Epinephrine treatment produced the same effects as swimming on blood sugar and lactic acid levels in normal animals. Adrenocortical extracts caused recovery from pantothenic acid-deficient hypoglycemic collapse but not from the similar riboflavin-deficient collapses. Thus increased sensitivity to insulin and to epinephrine appeared present in riboflavin deficiency and increased insulin sensitivity, normal response to epinephrine but hypocorticalism in pantothenic acid deficiency.

Fasting blood lactic acid levels rose 100% in 11–13 weeks in riboflavin-deficient dogs as did in lesser degree blood pyruvic acid. Eosinopenia was marked also in this deficiency but eosinophilia characterized late pantothenic acid deficiency. Swimming stress caused excessive rises in blood glucose and lactic acid in riboflavin-deficient but not in pantothenic acid-deficient and normal dogs. Marked eosinopenia was caused by swimming in the normal but not in any of the deficient animals. The normal and pantothenic acid-deficient dogs, following epinephrine treatment, showed the usual rise and fall in blood glucose and lactic acid, increased liver glycogen and marked eosinopenia. Cortisone treatment produced lowering of glucose and lactic acid blood levels in normal and riboflavin-deficient dogs but a rise in glucose in the pantothenic acid-deficient animals. Enlarged and hemorrhagic adrenals of lowered ascorbic acid content were usually found in the severely riboflavin-deficient dogs but significantly fatty livers only in the animals which had succumbed in hypoglycemic collapse. The pantothenic acid-deficient dogs had adrenals of nearly normal composition in spite of hemorrhagic lesions and moderately fatty livers. The adrenal cholesterol was normal in both deficiencies. In riboflavin-deficiency in both stressed and unstressed conditions, dogs manifest some signs of hypoxia, hypersensitivity or over-production of epinephrine but no adrenal cortical failure. Pantothenic acid-deficient dogs show little evidence of hypoxia or epinephrine sensitivity but signs of hypocorticalism.

The interrelationships of dietary vitamin E and essential fatty acids and their effects on serum and pulmonary prostaglandin (PG) synthesis and fatty acid precursors were examined. In a preexperimental period, male weanling rats were depleted of essential fatty acids (EFA) by feeding on a hydrogenated coconut oil diet. At the end of 45 days, average serum triene:tetraene ratio for the EFA-deficient rats was 0.76. After a refeeding period with a 20% safflower oil diet and 0, 1 or 50 mg of dl-alpha-tocopheryl acetate daily, serum and pulmonary fatty acid profiles and PG synthesis were determined. A trend to growth depression on the high vitamin E diet was observed. Vitamin E supplementation seemed to have no significant effect on fatty acid composition or synthesis of PGE1, PGE2, PGF2 alpha or PGI2 in lung. This may be due to the small lipid content and presumed inability of lung to accumulate excess vitamin E. Lung may, therefore, be resistant to such dietary manipulations. Serum PG synthesis was not affected by vitamin E dose, although the C20:4 omega 6/C18:2 omega 6 ratio in serum was significantly lowered on the high vitamin E diet.

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