Abstract
In earlier reports from this laboratory 1 , 2 a progressive paralysis was described in dogs subsisting on a diet lacking some members of the B complex and very low in potassium, 0.006%. This paralysis was invariably fatal if untreated and ran its course in 12-24 hours after the progressive stage was established. The mineral lack was suspected as a contributing cause, but since the first dog treated with potassium chloride, 700 mg total dose (55 mg/kg), failed to improve and later responded to 1 mg total dose (80 μg/kg) of synthetic biotin, we then centered our attention on the significance of biotin.
While this work was in progress, Elvehjem and his colleagues 3 succeeded in curing with much larger doses of potassium several dogs that had become paralyzed while subsisting on the same deficient diet. Consequently, the next 3 dogs to become paralyzed in this laboratory were treated orally with potassium chloride in much larger doses, 2-5 g total dose (200-500 mg/kg) as compared with the 0.7 g (55 mg/kg) used in the first unsuccessful treatment. This dose level proved entirely adequate, resulting in prompt and complete reversal of the paralytic process.
There is a marked difference in the therapeutic effects of potassium and biotin on the paralysis even in the same animal (Fig. 1). In making therapeutic tests, only animals that had reached the progressive stage of the paralysis were used. In our experience, animals with neck symptoms only are subject to spontaneous recovery, and, therefore, are not reliable for such tests. The paralyzed animal is usually somewhat emaciated, markedly dehydrated, anuric and suffers from complete anorexia during the attack. After treatment with either biotin or potassium chloride and about the time there is evidence of clinical improvement, copious urination occurs.
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