236 /• /• Christian 



stated that this reaction was a "model of a thyrotrophic alarm reaction." 

 His evidence was, for the most part, indirect and his conclusions that there 

 was increased thyroid activity on the basis of increased renal excretion of 

 injected radioiodine is untenable, especially for animals with a marked 

 increase in adrenocortical activity. Finally, Brown-Grant et al. (1954b) 

 found that the release of radioiodine by the thyroids of wild rabbits was 

 inliibited by emotional stress, just as it was in the usual domestic rabbit. 

 In view of these facts, the concept of a "fright thyrotoxicosis" is inaccepta- 

 ble. The inhibition of thyroid activity by emotional stress was not as 

 consistent in adrenalectomized as it was in intact rabbits, otherwise their 

 responses were similar. There is little doubt that the inhibition of thyroid 

 activity in these experiments was due to a decrease in the secretion of 

 thyrotropin (Brown-Grant et al., 1954a, b). It is true that cortisone and 

 ACTH inhibit the release of TSH from the pituitarics of rats (Brown- 

 Grant, 1955) and rabbits (Brown-Grant ct al., 1954a, b; Harris and Woods, 

 1958), but the adrenal corticoids cannot be responsible for the major part, 

 if any, of the inhibition of the release of thyrotropin in the above experi- 

 ments, as adrenalectomy did not affect the inhibition of the thyroid, and 

 cortisone was without effect on the release of radioiodine by the thyroids 

 of rabbits injected with TSH. Finally, injected TSH abolishes the inhibition 

 of the thyroid produced by ACTH and cortisone (Harris and Woods, 1958) . 

 There has been some confusion in the literature about the effect of 

 alarming stimuli on the thyroid. The experiments which have been dis- 

 cussed so far indicate that the thyroid is depressed under these circum- 

 stances, but it is also well known that emotional factors can precipitate 

 thyroid crises in humans (Selye, 1950). These apparently contradictory 

 experiences may depend on species differences, dose-time relationships, or 

 both, as the recent work of Gerwing et al. (1958) has indicated. These 

 investigators have shown that thyroid activity in mice, rats, and rabbits 

 subjected to chronic toxic "stress" (injection of small doses of bacterial 

 endotoxins repeatedly for 24 days) is inhibited at first, but returns to 

 normal and eventually exceeds the original normal level as the stimulation 

 continues (Gerwing, 1958; Gerwing et al, 1958) . On the other hand, guinea 

 pigs and rhesus monkeys exhibit increased thyroid activity from the be- 

 ginning. Injected thyrotropin stimulates the thyroids of mice, rats, and 

 rabbits with inhibited thyroids following injection of the toxin, indicating 

 that the depressed thyroid function was due to a diminished secretion of 

 TSH. It may be coincidental, but it is nevertheless interesting that these 

 differences in thyroid function between species in response to bacterial toxin 

 coincide with the differences in the secretory patterns of the major corti- 

 coids in these same species (cf. above) : rats, mice, and rabbits secrete pri- 

 marily corticosterone, and the other two species, hydrocortisone. These 



