Mechanisms Controlling Ovulation of Avian and Mammalian Follicles 129 



of follicles. The distinction then is that during the hormone-adequate phase 

 follicles are capable of rapid growth but are incapable of ovulating, while 

 during the hormone-inadequate phase they are in a stage of physiological 

 atresia when they can be made to ovulate because they are physiologically 

 essentially "inactive". If follicles remain without adequate gonadotropic 

 support too long, physical atresia sets in and they become incapable of 

 ovulating for obvious reasons. 



The stage of "physiological atresia" which, according to the theory pro- 

 posed, is viewed as being due to a deficiency of gonadotropic hormone is 

 relatively prolonged, lasting days in mares and rabbits, and hours in other 

 mammals and in chickens. It is also distinguished by the fact that during 

 this phase follicles can ovulate at any time after they receive the LH-born 

 signal to do so. This view is supported by the experimental evidence presented 

 which shows that follicles, which have become ovulable as a result of hormone 

 withdrawal following hypophysectomy, can be made non-ovulable if they 

 receive support in the form of small or moderate doses of FSH-containing 

 hormones which presumably prevent them from becoming "physiologically 

 atretic" and hence ovulable. 



The question now arises what physiological changes take place in the follicle 

 wall and especially in the stigma of follicles which are in the phase of physio- 

 logical atresia and which have received the signal that ovulation shall occur 

 about ten hours later. 



The tentative theory is proposed that the effect of LH may be that of 

 causing either general follicular ischemia, or local ischemia which is restricted 

 to the stigma of follicles. In normal hens ovulation is demonstrably preceded 

 by a blanching of the wall of the follicle destined to ovulate, the stigma widens 

 measurably and the capillaries extending across it constrict. Eventually a 

 small rip appears in one corner of the stigma and the ovum bulges through it. 

 The rip widens and the ovum slips out of the follicular sac which collapses. 

 These conclusions are based on subjective but numerous observations which 

 do not lend themselves easily to quantitative measurements. Experiments 

 now in progress are designed to test the theory that ovulation is the result 

 of ischemia, although it is recognized that if ischemia is restricted to the 

 stigma area of the follicle, it will be difficult to measure minor differences in 

 the amount of blood present, especially in the smaller mammalian follicles. 



In laying hens the mature follicle may be maintained in the ovulatory 

 state over prolonged periods of time. In hypophysectomized hens this can 

 be done by supporting the mature follicle with FSH-containing hormones. If 

 the dose of supporting hormone injected is chosen correctly, the follicle will 

 not ovulate nor will it become atretic. However, if an ovulatory dose of LH 

 has been administered to hens containing follicles which have reached the 

 "physiological atresia" stage, their ovulation cannot be prevented if support- 

 ing FSH treatment is begun at the time of hypophysectomy. These as yet 



