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From the Department of Obstetrics and Gynecology, College of Physicians and Surgeons, Columbia University NEW YORK CITY
Abstract
Reid Hunts observation that white mice treated with thyroid substance showed an increase in their resistance against acetonitril, gave us a very suitable method for the study of thyroid disturbances. Hunt considers the protective action as due to acceleration of the oxidation of acetonitril, formic acid and thiocyanate. In all probability the mechanism of detoxication is more complicated. A diminution of the effect of the poison results. Numerous writers (Ghedini, Gellhorn, Miura, Reid Hunt, von Bergmann and others) found that this reaction was not specific for the thyroid but could also be produced by other organ extracts. With the increase in knowledge of the endocrines the reason for this peculiar behavior becomes clearer. It offers an explanation of why the administration of the serum of pregnant women or anterior pituitary gland extracts increases the resistance to acetonitril. Thyroxin and the thyrotropic hormone are responsible for the elevated Reid Hunt reaction. Animal tests have shown unquestionable histological changes in the thyroid after the administration of the serum of pregnant women (Schenk) in the form of stimulation. A further proof for the activation of the thyroid during pregnancy was given by Eufinger and Wiesbader who demonstrated the acceleration of metamorphosis of frog larvae after the addition of serum of pregnant women.
The following experiments show the effect of serum of normal subjects, serum of pregnant women in the ninth and tenth months of pregnancy, of anterior pituitary-like hormones (follutein) and the thyrotropic hormone.
Footnotes
1 This work was supported by a grant from E. R. Squibb and Sons.
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