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Since exogenous progesterone (P4) causes superovulation in hypophysectomized (hypoxed) cyclic hamsters treated with gonadotropins, the current study was performed to evaluate the roles of P4and luteinizing hormone (LH) as a folliculotropic complex in the immature hamster. Intact or hypoxed immature hamsters were injected daily, beginning on Day 23, with 1 mg P4and/or 20 μg LH for 4 days. Treatment with P4alone or combined with LH in intact immature hamsters increased the number of antral follicles (6.7 and 43, respectively, vs. 1.5 per ovary in controls), but neither treatment maintained large follicles in hypoxed animals. In contrast, in hypoxed hamsters, the number of small preantral follicles was enhanced by P4or LH (406 and 409, respectively, compared to 302 per ovary in untreated controls), but with no additive effects by combined treatment. The stimulatory effect of P4in intact hamsters was unrelated to serum levels of follicle-stimulating hormone, estradiol, or LH. Moreover, in the hypoxed hamster, P4or LH acts directly to increase the numbers of small preantral follicles with 2 to 5 layers of granulosa cells, whereas equally large doses of stilbestrol or estradiol cyclopentylpropionate are infective. In the hypoxed or intact hamster, the effects of P4or LH may involve either recruitment of smaller follicles into larger stages or prevention of atresia. The present experimental design can not distinguish between these possibilities.

A synchronous population of atretic follicles was produced in hypophysectomized hamsters on the day of ovulation (Day 1) by injecting them immediately s.c. with pregnant mare’s serum (PMS) followed by an i.p. injection of PMS-antiserum at 0900 h on Day 4. At various times thereafter isolated follicles were exposed in vitro to different doses of ovine luteinizing hormone (LH) (0 to 200 ng) and incubated for 1 h. Cyclic AMP (cAMP), estradiol (E2), testosterone equivalent (T), 17α-hydroxyprogesterone (17-OH-P) and progesterone (P) were then measured. At 0900 h of Day 4, nonatretic follicles (not injected with PMS-antiserum) showed the highest level of cAMP, P and 17-OH-P in response to stimulation by 7 and 200 ng of LH. E2and T were lowest in the groups incubated with no LH or with 200 ng/ml of LH and highest when stimulated by 7 ng.Atretic follicles showed a graded response to LH depending on the degree of atresia. By 12 h following injection of anti-PMS, none of the doses of LH produced significant increases in E2or T; however, 200 ng of LH stimulated significant increases in P (1 ng increase) and 17-OH-P (564 pg increase) and increased cAMP above control levels (7.3 ± 1.6 pmol vs. 2.6 ± 0.2 pmol, respectively). By 24 h, with 200 ng LH, follicular 17-OH-P declined to control levels present at Time zero, followed by a fall in P at 48 h and cAMP at 72 h. Cyclic AMP and steroid levels were directly influenced by the dose of LH and the degree of atresia (P<0.0001).These studies indicate that with this model atretic follicles rapidly lose their ability to synthesize E2and T while production of 17-OH-P, P and cAMP declines more slowly as atresia advances. Based on previous studies of others we postulate that the early breakdown of the granulosa may cause the initial drop in E2and T while the theca continues to produce 17-OH-P, P and cAMP until more advanced stages of atresia.

To determine the mechanisms responsible for the suppression of follicular development in the lactating rat, in vivo and in vitro determinations of steroid and peptide hormones combined with the histological size-distribution of ovarian follicles were compared among three groups of post-parturient rats nursing 0, 2 or 8 pups. From Days 4 to 12 (day of parturition = Day 0 of lactation), in dams nursing 8 pups, follicles larger than 401 µM in diameter were absent, whereas follicles of this size were always present in mothers nursing 0 or 2 pups. The in vitro production rates of estradiol-17β(E2) and testosterone (T) by nonluteal ovarian tissues (NLO) were consistently lower in dams nursing 8 pups than in mothers nursing 0 or 2 young, correlating with the histological observations. Serum E2and 20α-dihydroprogesterone (20α-OHP) in rats with 8 pups were significantly lower, whereas serum progesterone (P) was significantly increased compared to the values in dams nursing 0 or 2 pups. In mothers nursing 8 pups, the corpora lutea (CL) of lactation, formed at postpartum ovulation, produced in vitro significantly greater amounts of P but significantly lesser amount of E2compared to the other groups. Serum luteinizing hormone (LH) was consistently lower in dams nursing 8 pups than in dams nursing 0 or 2 pups. There was, however, no significant difference in serum follicle-stimulating hormone (FSH) among the 3 types of postparturient rats. Throughout lactation serum values of FSH were within the range of diestrous levels during the estrous cycle. Serum levels of prolactin (Prl) in dams nursing 8 pups were strikingly higher compared to dams nursing 2 pups. The administration of small doses of human chorionic gonadotropin (hCG) or ovine LH twice daily from Days 2 to 5 to lactating rats nursing 8 pups induced the maturation of follicles capable of ovulating.These findings indicate that during the first half of lactation the strong suckling stimulus reduces serum LH directly or indirectly via high levels of serum Prl and P, which in turn inhibit follicular maturation. During the second half of lactation, the suckling stimulus wanes, Prl and P decline and serum LH recovers to basal cyclic values which are reflected in the initiation of follicular maturation.

This study was designed to determine whether the major site of eCG neutralization by an antiserum to the hormone is at the peripheral or ovarian level. Hamsters hypophysectomized at oestrus were injected s.c. with 25 iu eCG. Three days later, preovulatory follicles were dissected and cultured for 5 h and the medium was changed every hour. At the end of the first hour of incubation, oestradiol and androstenedione accumulation was high, with a sharp drop over the next 4 h, whereas progesterone concentrations did not change over the entire period. Addition of eCG antiserum to the incubated follicles did not affect steroidogenesis. Addition of 1.0 iu eCG in the second hour or every hour sustained oestradiol production at supraphysiological amounts. However, addition of eCG plus eCG antiserum every hour eliminated the stimulatory effects of eCG on oestradiol production. In another experiment, hamsters injected with eCG were treated 3 days later by i.p. injection of eCG antiserum and groups of animals were killed over the next 8 h. Serum samples before and after injecting eCG antiserum were incubated overnight with a goat anti-rabbit immunoglobulin to separate free, unbound eCG from bound eCG. At time zero (before injecting the antiserum) free eCG was increased, but within 1 h after eCG antiserum there was an eightfold decrease of the hormone, and these concentrations were maintained over the next 7 h. The fall in unbound eCG in vivocoincided with the decay in serum oestradiol and androstenedione. These results obtained in vitroand in vivodemonstrate that the long biological half-life of eCG is essential to replenish the supply provided to the ovary constantly to maintain steroidogenesis; eCG antiserum inactivates eCG in serum but not by complexing with eCG at the receptor of the follicular cell surface.

Summary.Immature rats and adult hamsters were killed on Days 2,4 or 8 of pregnancy (Day 1 = sperm positive vaginal smear). Dispersed luteal cells (5 × 104cells) were incubated for 2 h in the absence or presence of graded doses of ovine LH. In the absence of LH, incubation of rat luteal cells compared to hamster cells produced about 3–6-fold as much progesterone, 26–66 times as much 20α-dihydroprogesterone and about the same amounts of 17α-hydroxyprogesterone. For the rat, 1 ng LH was the minimal dose which stimulated synthesis of progesterone and 17α-hydroxyprogesterone by luteal cells on Days 2 and 4 whereas 10 ng LH stimulated maximal production of progesterone by Day-8 luteal cells. As pregnancy progressed from Day 2 to Day 8, there was an inverse relationship between the levels of progesterone and 20α-dihydroprogesterone accumulated by rat luteal cells. For the hamster, 1 ng LH significantly stimulated accumulation of progesterone and 17α-hydroxyprogesterone by Day-2 luteal cells but not by Day-4 or Day-8 cells. Hamster luteal cells on Day 4 produced the highest levels of progesterone in response to 10 or 100 ng LH, with a maximal rate of accumulation by Day-8 cells with 10 ng LH.

Summary.Hypophysectomized PMSG-primed hamsters were injected with PMSG antiserum and the theca and granulosa cells of the resulting atretic follicles were incubated in vitro. In the absence of added hormone, 17α-hydroxyprogesterone and oestradiol production was not detectable in granulosa cells collected and incubated at 0, 12 and 24 h after antiserum. Progesterone production was not detected in control incubations at 0 h but was measurable with cells collected at 12 h after PMSG antiserum. When incubated with androstenedione or pregnenolone (10 ng/ml for each) 17α-hydroxyprogesterone and progesterone production by granulosa cells were significantly increased at 0, 12 and 24 h after antiserum. Granulosa cells were capable of aromatizing androstenedione to oestradiol at all times examined. At 0 and 12 h after antiserum to PMSG, isolated thecal shells produced androstenedione. LH stimulation caused increased androstenedione production in all thecae at 0 h, in 50% of the thecae at 12 h and in none at 24 h after antiserum. Thecal shells produced 17α-hydroxyprogesterone in response to LH at 0,12 and 24 h after antiserum, and produced progesterone at all times examined. Thecae also responded to LH with increased progesterone production up to 72 h after antiserum. These experiments demonstrate that one important steroidogenic event in atresia may be the loss of activity of C 17,20 lyase in the theca leading to loss of substrate (androstenedione) for granulosa cell aromatization, although aromatase activity is present until at least 24 h after the induction of atresia.

Summary.To assess the roles of FSH and LH on follicular growth, after various experimental manipulations, hamster follicles were sorted into 10 stages and incubated for 4 h with [3H]thymidine. Stages 1–4 correspond to follicles with 1–4 layers of granulosa cells, respectively; Stage 5 = 5 or 6 layers of granulosa cells plus theca; Stage 6 = 7–8 layers of granulosa cells plus theca; Stage 7 = early formation of the antrum; Stages 8–10 = small, intermediate and large antral follicles, respectively.Phenobarbitone sodium injected at 13:00 h on pro-oestrus blocked the normal rise of blood FSH and LH concentrations at 15:00 h and prevented the increase of [3H]thymidine incorporation into follicles of Stages 1–9. The optimal treatment to reverse the effects of phenobarbitone was 1 μg FSH and 2 pg LH injected i.p. at 13:00 h which restored DNA replication to follicles of Stages 2–10: FSH acted primarily on Stages 2–5 and LH on Stages 5–10. Injection of phenobarbitone at 13:00 h on prooestrus followed by 2·5 μg FSH at 22:00 h restored DNA synthesis by the next morning to follicles at Stages 1–8. In hamsters hypophysectomized at 09:00 h on the day of oestrus (Day 1), injection on Day 4 of 2·5 μg FSH restored DNA synthesis 6 h later to Stage 2–6 follicles. Unilateral ovariectomy on Day 3 resulted 6 h later in an acute rise in FSH and LH and change of follicles from Stage 4 to Stage 5 but, paradoxically, there was decreased synthesis of DNA in follicles of Stages 5–10. The incorporation of [3H]thymidine was at normal low levels for Stage 5–10 follicles by 24 h after unilateral ovariectomy with significant increases in follicles of Stages 1–4. We conclude that small preantral follicles are already dependent on FSH for DNA synthesis and LH action is manifested when the follicles acquire a theca (Stage 5 onwards) and when LH receptors appear in granulosa cells.

Summary.Hamsters injected s.c. on the day of ovulation (Day 1) with 100 μl equine anti-bovine LH serum ovulated 28 eggs at the end of a 5-day cycle. When a second injection of anti-LH serum was administered 4–93 days later, the animals did not superovulate and had normal 4-day cycles. Injection of 100 μl normal rabbit serum (NRS) on Day 1 followed 14 days later by anti-LH serum resulted in the ovulation of 32 ova whereas a priming injection of 100 μl normal horse serum (NHS) followed by anti-LH serum resulted in the ovulation of only 18 ova. When hamsters were injected on Day 1 with anti-LH serum, NHS or NRS and then with anti-LH serum in the 4th cycle, high titres of free antibodies to LH were present on Days 2–4 only in the animals treated with NRS; these hamsters ovulated a mean of 35 ova.These experiments suggest that the hamster rapidly forms antibodies to equine immunoglobulins, thus preventing a second injection of anti-LH serum from inducing superovulation.

Measured by radioimmunoassay, the peripheral plasma oestradiol concentration reached a peak (21·2±1 pg/ml) between 10.00 to 12.00 hours on Day 4 of pregnancy in mice. These values were significantly different from all others measured between 07.00 and 18.00 hours. To determine the physiological significance of this peak, ovariectomies were performed at selected intervals. Ovariectomy at 08.00 hours or earlier usually prevented implantation. The period from 10.00 to 12.00 hours on Day 4 was found to represent a critical time period before which insufficient oestrogen is secreted, in most instances, to initiate implantation.

The steroidogenic abilities of the newly formed corpus luteum (8–10 h after ovulation) and the non-luteal ovary were compared in the guinea-pig, hamster, rabbit and rat using an invitro incubation technique. Histologically, newly formed rat corpora lutea (CL) were highly luteinized whereas the CL of the rabbit and guinea-pig were only partially luteinized. The CL of the hamster showed the least amount of luteinization.Serum progesterone was highest in the rat (18 ± 3 (s.e.m.) ng/ml). In the hamster, it was about 8 ng/ml, whereas in the rabbit and guinea-pig it was about 1 ng/ml. Serum androstenedione ranged between 0·5 and 1 ng/ml. Serum testosterone was lowest in the hamster (60 pg/ml) and highest in the rabbit (470 pg/ml), whereas in the rat and guinea-pig, testosterone levels were similar (about 240 pg/ml). Serum oestrogens were at baseline levels in all species.The CL of the rat exhibited considerably greater steroidogenic ability than the CL of the other species, producing 70 ± 6 ng progesterone/mg per h, 215 ± 14 pg androstenedione/mg per h, 49 ± 3 pg testosterone/mg per h, 3 pg oestrone/mg per h and 1 pg oestradiol/mg per h. Rabbit CL produced only progesterone (7 ± 2 ng/mg per h). Newly formed hamster CL produced none of the above steroids. In general, the ability of the CL to produce progesterone in vitrocorrelated with the degree of luteinization found by histological observation. Guinea-pig CL were embedded deeply in the ovary and could not be obtained without damage. Consequently, a portion of the ovary containing a corpus luteum was incubated. There was no difference in the steroid production by this portion of the ovary compared with the non-luteal ovary.The non-luteal ovary of the rat produced the highest amount of progesterone (10 ± 2 ng/mg per h). The guinea-pig non-luteal ovary produced about 5 ± 2 ng progesterone/mg per h, whereas the non-luteal ovary of the rabbit did not produce any. On the other hand, the hamster non-luteal ovary lost progesterone. Non-luteal ovaries from all species produced androgens. The non-luteal ovary of the guinea-pig contained especially large numbers of atretic antral follicles. The guinea-pig non-luteal ovary produced extremely large amounts of androstenedione (1110 ± 210 pg/mg per h) and testosterone (606 ± 154 pg/mg per h) compared with the amounts produced by the non-luteal ovary of the rat, hamster and rabbit. In the non-luteal ovary, interstitium and atretic antral follicles are the probable source of androgens.Oestrogen production by the non-luteal ovary was at baseline levels in the four species studied correlating with the absence of healthy antral follicles. The results indicate the extreme species differences that exist in ovarian function in the early postovulatory period.

Progesterone was secreted by hamster corpora lutea between days 1 and 15 of pregnancy; on day 14, the concentration in the peripheral plasma reached a maximum. A pronounced fall in luteal weight began on the day after parturition and the corpora lutea had virtually disappeared by days 4–5 post partum. The concentration of protein and the weights of the corpora lutea reached peak levels on days 12 and 14 respectively. The highest levels of luteal RNA were reached on days 12–13. The concentration of DNA in the corpora lutea was constant throughout pregnancy, indicating that hypertrophy rather than hyperplasia accounted for the increase in luteal weight.Luteal concentrations of cholesterol and its esters were unchanged between days 1 and 14 of pregnancy except for a significant decline in the level of cholesteryl ester on days 8 and 13. During the final stages of regression of the corpora lutea during lactation, the luteal concentrations of free and esterified cholesterol rose to three and ten times respectively, the values obtained on day 2 of pregnancy. A significant increase in the concentration of acid and alkaline phosphatase began on day 16 of pregnancy correlated with the onset of structural luteolysis.The activity of luteal glucose-6-phosphate dehydrogenase peaked on days 2 (comparable to the value on day 2 of the oestrous cycle) and 13 of pregnancy and day 3 of lactation. The high levels on these days may be associated either with luteal steroidogenesis during pregnancy or with lipid metabolism during the post-partum involutional phase. The activity of luteal 3β-hydroxysteroid dehydrogenase was relatively constant except for significant decreases on days 10 and 13 of pregnancy.The results indicate that the activities of all of the biochemical variables in the corpora lutea of pregnancy were highest between days 11 and 13.

Pregnant rats were injected s.c. with antiserum to LH (anti-LH) on days 8 or 10 of pregnancy (day 1 = day of sperm-positive vaginal smear) and subsequently given various steroids s.c. to prevent luteolysis and/or abortion. A single injection of 4 mg progesterone on day 8 prevented abortion and luteolysis as shown on day 12 by the presence of fetal swellings and levels of progesterone in serum (88 ±6 (s.e.m.) ng/ml) and corpora lutea (26±3 ng/mg) comparable to control values. After 0·5 ml anti-LH on day 10, a daily dose of 4 mg progesterone prevented abortion in five out of eight animals but by day 13 luteal progesterone was 3·0 ± 0·7 compared with 24±3 ng/mg in controls.After anti-LH on day 8 or 10, daily injections of 1 or 4 mg testosterone propionate or 10 μg, 100 μg or 1 mg oestradiol failed to prevent abortion or to raise luteal concentrations of progesterone to normal values. However, 4 mg testosterone propionate on day 8 or 100 or 500 μg oestradiol on day 10 maintained serum progesterone levels at approximately half those of control values. Treatment with 4 mg testosterone propionate on days 8–11 led to significant increases in serum and luteal levels of testosterone and oestradiol on day 12; on day 10 exogenous oestradiol (100 or 500 μg) increased serum and luteal levels of oestradiol by day 13.These results, especially treatments begun on day 8, are difficult to reconcile with the current concept that the luteotrophic action of LH in the pregnant rat is exerted by increasing luteal androgens that are aromatized to oestrogens which then act as the direct luteotrophic stimulus.

The corpora lutea (CL) of the hamster secrete progesterone on days 1 and 2 of the oestrous cycle before marked regression at pro-oestrus (day 4) virtually eliminates them from the ovary. Luteal protein and RNA reached their maximum values on day 2 and declined up to day 4. DNA was constant throughout the cycle substantiating the importance of cellular hypertrophy rather than hyperplasia in the growth of the CL. Concentrations of cholesterol and its esters were unchanged between days 1 and 3 but almost doubled in concentration on day 4.Glucose-6-phosphate dehydrogenase activity was maximal on days 2 and 4, apparently associated on these days with steroidogenesis and lipid metabolism, respectively. A significant increase in acid phosphatase activity occurred on day 3 reaching maximal values on day 4, probably accounting for the rapid regression of the CL. The maximal concentration of 3β-hydroxysteroid dehydrogenase in CL was on day 1, with a gradual decline over the next 3 days.

Summary.As measured by radioreceptor assays, binding sites for FSH and prolactin were present at 09:00 h on the day of pro-oestrus in Stage 1–10 follicles (primary to antral) with prolactin receptors 3–6 times higher than FSH sites in Stages 1–3 (3 layers of granulosa cells). Specific binding sites for hCG were present in Stage 1 and 2 follicles (2 layers of granulosa cells) but thereafter their distribution was erratic and they were not consistently detectable until Stage 5, when thecal cells first appeared. Using topical autoradiography, specific binding for FSH was evident in Stage 1–4 follicles (4 layers granulosa cells) whereas specific hCG-binding was not. After the preovulatory gonadotrophin surges, by 21:00 h on pro-oestrus, FSH receptors declined in Stages 5–10, prolactin receptors fell in Stages 8 and 10 (small and large antral follicles) and hCG receptors were reduced in Stages 7 (start of antral cavity) to 10. On the morning of oestrus, for follicles from Stage 4 onwards, receptor numbers usually returned to levels found at 09:00 h on pro-oestrus. At oestrus, the few remaining Stage 10 follicles were all atretic and contained significantly reduced FSH and prolactin receptors but numbers of hCG binding sites comparable to those at 09:00 h of pro-oestrus. These results provide evidence of gonadotrophin receptors in small primary and secondary follicles which is consistent with increased DNA synthesis in small hamster follicles on the afternoon of pro-oestrus and on the morning and afternoon of oestrus. Periovulatory changes in gonadotrophin concentrations may therefore affect early stages of folliculogenesis.

Summary.Collagenase-dispersed interstitial cells from 5-day hypophysectomized hamsters produced progesterone (81 ± 7 pg/10 000 viable cells/2 h incubation) and responded to ovine LH stimulation in vitrowith a dose-dependent increase in progesterone. FSH and prolactin had no effect. The interstitial cells did not produce detectable levels of oestradiol, oestrone, androstenedione, 17α-hydroxyprogesterone or 20α-dihydroprogesterone although 17α-hydroxyprogesterone production rose to 26 ± 5 pg/10 000 cells/2 h in response to 25 ng LH/ml. Isoproterenol (500 ng/ml) and epinephrine (500 ng/ml) stimulated progesterone production and this response was blocked by concurrent administration of 6 × 10−6m-propanolol which had no effect on LH-stimulated progesterone production. Simultaneous LH and catecholamine stimulation did not produce an additive effect. Incubation in medium containing 10% serum from hypophysectomized animals did not affect progesterone production. The addition of 10−6m-d-ala6-LHRH to interstitial cells resulted in a significant reduction of baseline steroidogenesis. These results suggest long-term retention of functional LH receptors and integrity of the steroidogenic pathway through progesterone despite chronic gonadotrophin deprivation and may indicate a role for the interstitium in priming follicular growth following periods of anoestrus.

Summary.Immediately after hypophysectomy, 30 i.u. PMSG were injected s.c. and 3 days later an antiserum to PMSG was injected i.p. Groups of hamsters were killed at 0, 24, 48 and 72 h after PMSG antiserum. The ovaries were prepared for topical autoradiography and the numbers of silver grains in different ovarian compartments were counted. The numbers of binding sites for 125I-labelled FSH in the granulosa cells of the antral follicles dropped sharply to 33, 14 and 5% of that at 0 h at 24, 48 and 72 h respectively. Binding of 125I-labelled hCG to granulosa cells declined more slowly, being 47, 27 and 24%, respectively. Binding of 125I-labelled hCG to thecal and interstitial cells was unaffected. Compared to other models of atresia, the changes in gonadotrophin binding observed in this model occur at an accelerated rate because of the acute deprivation of PMSG.

Summary.Atresia was induced in antral follicles of hypophysectomized PMSG (30 i.u.)-treated hamsters by an i.p. injection of PMSG antiserum. Mature antral follicles were isolated and incubated for 1 h. When expressed per follicle, cAMP increased 108% above control levels at 2 h, while cGMP rose 117% at 4 h; both nucleotides then declined (12–72 h). DNA per follicle fell below control values by 24 h and reached its lowest point at 48 h. Serum concentrations of oestradiol-17β and testosterone were 50% lower by 1 h after injections of PMSG antiserum. Oestradiol and testosterone in serum, incubation medium and tissue dropped rapidly to reach basal values by 12 h. Serum progesterone showed a sharp increase at 4 h then dropped below control levels by 12 h and remained constant thereafter. In tissue and medium, progesterone rose to peak values at 8 h, then dropped to control levels with no significant changes for the remaining 64 h. The precipitous decreases in both oestradiol and testosterone in the serum, medium and tissue indicate inhibition of steroid synthesis at some point after progesterone formation.These results demonstrate the usefulness of this model for following atretic changes in a synchronized population of Graafian follicles.

An acid extract of human neutrophil granules was fractionated on a Sephadex G-100 column and tested for microbicidal activity against Acinetobacter calcoaceticus HO-1 as described previously (M.C. Modrzakowski and C. M. Paranavitana, Infect. Immun. 32:668-674, 1981). The low-molecular-weight protein fraction, peak D, accounted for about 30% of the protein and nearly all of the activity of the crude extract against strain HO-1. Peak D protein proved to be a mixture of the three human defensin peptides HNP1, HNP2, and HNP3. Purified defensins reproduced the microbicidal activity of peak D. The data suggest that defensins could play a major role in the killing of A. calcoaceticus by human neutrophils.

When hamsters were hysterectomized on day 1 of pregnancy, ovulation occurred 17 days later. On day 12 of this prolonged pseudopregnancy, plasma levels of progesterone were approximately half of those of intact animals on the same day of pregnancy. The concentration of follicle-stimulating hormone in the pituitary of the hysterectomized animals was only half that of the pregnant group, but luteinizing hormone concentrations were similar. The massive proliferation of antral follicles characteristic of pregnant hamsters on day 12 was not found in the hysterectomized animals; injection of 20 i.u. human chorionic gonadotrophin (HCG) on day 12 resulted in the ovulation of 31 and 6 ova respectively, but priming the hysterectomized hamsters with pregnant mare serum gonadotrophin (before HCG) resulted in superovulation.After hysterectomy on day 9 of pregnancy, by day 12 there was a rapid decline in luteal activity as shown histologically by the onset of structural luteolysis and a concomitant fall in luteal weight, and luteal and plasma levels of progesterone. These effects were partially or completely reversed by daily injection of 1 mg prolactin on days 9–11.The results indicate that hysterectomy before the establishment of the placenta results in the sustained release by the pituitary of prolactin and gonadotrophins, but most likely at lower levels than in pregnant animals. However, hysterectomy on day 9 abruptly removes the placental source of a prolactin-like hormone and the pituitary cannot respond in time to prevent luteolysis.

The concentrations of follicle-stimulating hormone (FSH), luteinizing hormone (LH) and prolactin in serum at 09.00 h on each day of pregnancy and 9 selected days of lactation in the hamster were determined by radioimmunoassays.The concentration of FSH on day 1 of the 16-day pregnancy was approximately fivefold greater than the levels on subsequent days. Concentrations of LH decreased on each of the first 3 days of gestation, rose slightly during mid-pregnancy, and then tended to decline during the last trimester. The concentration of prolactin increased approximately twofold from day 1 to day 3, remained elevated until day 8, and then gradually returned during the last half of gestation to the level on day 1. The concentrations of the three hormones on the first 4 days of pregnancy differed markedly from the concentrations during the oestrous cycle.Parturition had occurred and lactation begun by 09.00 h on day 16 of pregnancy (day 1 of lactation) and the levels of hormone on this day were unchanged from the levels on day 15 of pregnancy. Thereafter, the concentration of FSH increased two- to fourfold while the levels of LH increased until day 3 but then returned to the levels found at day 1. Concentrations of prolactin remained unchanged after day 1 of lactation, except for a decrease on day 2.