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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.

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