Factors Influencing Ovulation and Atresia of Ovarian Follicles 215 



theca interna forming the wavy line tliat will become the hyaloid membrane . 

 of later atretic follicles. 



The same process probably occurs in human ovaries, although there is not 

 yet available today sufficient material to follow the same stages as closely. 

 The most striking feature of these observations for the present discussion is * 

 the hypertrophy of theca interna that appears coincident to the earliest sign 

 of atresia in those follicles of second rank. This feature occurs coincidentally - 

 with the formation of the first polar body or second maturation spindle of 

 the mature follicle about to ovulate. Incidentally, a careful study of rat ovaries 

 under various stimuli fails to reveal any theca interna thickening coincidental 

 to the cleavage of the ovum that typifies early atresia in this species. The 

 absence of this theca interna thickening in an animal that can readily accom- 

 modate an average litter of nine in comparison with its presence as seen in 

 the monkey in the eight to ten follicles wiped out each month, might lend 

 suggestive support to the thesis that the factors causing this theca hypertrophy 

 in the primate may be responsible in some way for the limitation of ovulation 

 to a single follicle each month. 



It is difficult to escape the probability that this clearly defined structure 

 plays some endocrine role in the cycle. Other endocrine events of consequence 

 are happening as well. The maturing follicle shows a tremendous spurt 

 of growth from day 12 to day 14 of the cycle. This is simultaneous with ' 

 the first high point in estrogen production during the menstrual cycle. In the 

 last 24 hr before ovulation, there is also a sudden surge of production of the 

 pituitary gonadotropin causing an LH effect. McArthur has documented * 

 such a peak in a normal cycle (3), and this has been confirmed by Taymor (4). 

 There is considerable evidence to suggest that the surge in estrogen produc- 

 tion by the spurting growth of the major follicle causes the release of this LH. 

 It may not even be estrogens themselves, but breakdown products that have 

 this result. Thus, if one castrates a rat and transplants one of the ovaries into 

 the spleen, the steroids produced by the transplanted ovary will be brought 

 in the portal circulation directly to the liver, and there become inactivated. 

 The continuing atrophy of the uterus in such a preparation confirms that 

 estrogens have not escaped into the general circulation from the liver. Yet, 

 the transplanted ovary becomes converted into an almost solid luteal body. 

 It seems probable in this case that the breakdown products of estrogen liberated - 

 from the liver are responsible for the LH and perhaps LTH coming from the 

 pituitary that causes such luteinization of the transplanted gonad (5). Now, 

 just as we have seen in the monkey that the period of theca hypertrophy in 

 atretic follicles is short lived, about two to four days, so also have studies * 

 shown that the peak of LH is hmited to the same time interval. It is unfortu- 

 nate that we do not have any evidence of this LH peak yet available from the 

 monkey nor do we have serial sections of sufficient human material to show 

 that the theca proliferation in the human is similarly a transient phenomenon. 



15 



