Day Of Diestrus Research Articles

L.D.H. and L.D.H. isoenzymes of the intra-uterine secretions of the cow during the estrous cycle

Abstract Uterine secretions were collected from 20 mature cows during estrus (day 0), metestrus (day 5), diestrus (day 10) and proestrus (day-1). Lactate dehydrogenase (LDH) and LDH isoenzymes activity were evaluated. No significant cyclic variations of LDH activity was found in the uterine secretions while the mean of the enzyme activity was higher during the estrogenic period of the cycle. The relative activity of LDH-1, LDH-2 and LDH-3 isoenzymes were higher during proestrus and estrus whereas LDH-5 activity was more important during metestrus. The LDH-3 seems to have the higher relative activity in uterine secretions of the cow.

Effects of Limiting Water Intake on the Rat Estrous Cycle with Observations on LH, Prolactin, and Corticosterone

By the fifth week of restricting water intake at 1100 to a 15-min period per day, estrous cycle lengths had shifted in most animals (31/40) from 4 to 5 days with the 5-day cycles usually consisting of 3 days of diestrus. In the 5-day cycling rats, plasma corticosterone peaked at 1100 and also at 1900 hr, the proestrous surge in plasma LH was not significantly changed, although the variation in individual animals was greater and the prolactin surge was prolonged. Similar prolonged cycles followed water restriction at 1800 hr with animals returning to regular 4-day cycles when given water to ad libitum. These results suggest that the alteration of the normal corticosteroid rhythm and/or changes in prolactin secretion may account, in part at least, for the changes noted in cycle length after restricting the water intake.

Termination at midpregnancy of the two daily surges of plasma prolactin initiated by mating in the rat.

The pattern of plasma prolactin following uterine cervical stimulation consists of two surges each day, one nocturnal, occurring between 0100-0900 h (lights on 0600-1800 h), and one diurnal, occurring between 1500-2100 h. This pattern of prolactin continued throughout pseudopregnancy; the last surge was observed on the morning of day 11 (day 1 was taken as the first day of diestrus of pregnancy or pseudopregnancy). Prolactin levels remained low thereafter until the spontaneous proestrous surge on the afternoon of day 12, signalling the onset of a new estrous cycle. In contrast, the two daily prolactin surges did not continue throughout pregnancy, and in fact, were terminated sooner in pregnant animals than in pseudopregnant animals. The last diurnal surge was observed on day 8 while the last nocturnal surge was observed on day 10. The early termination of prolactin surges during pregnancy correlated with the increased secretion of rat placental lactogen. However, placental extracts obtained from day 11 of pregnancy and injected in large doses failed to inhibit prolactin surges in pseudopregnant animals. Prolactin surges also continued for a longer period of time in pseudopregnant rats bearing decidualized uteri than in pregnant animals. Thus, the two major components of pregnancy that differed from pseudopregnancy, that is, the presence of rat placental lactogen or decidual tissue, did not appear to account for the early termination of prolactin surges during pregnancy.

Prolactin release by synthetic luteinizing hormone-releasing hormone (LHRH) in thyroidectomized-androgenized adult rats.

Synthetic LHRH, at a dose of 5 mug/kg, induced a marked increase in the serum LH level but a marked decrease in the serum prolactin level when injected iv to normal adult female rats on the day of estrus. In adrogenized adult rats which had been showing persistent estrous vaginal smears, a less marked increase in the serum LH level was shown following injection of LHRH. Prolactin level decreased only slightly in these animals. Control level of serum prolactin in normal estrous and androgenized rats were 4.95 +/- 0.35 and 5.42 +/- 0.65 mIU/ml, respectively. Thyroidectomized-normal cycling rats responded to LHRH with a slight decrease in the serum prolactin level when injected on the day of diestrus. Prolactin level increased, however, 5 min after LHRH injection in thyroidectomized-androgenized adult rats, which were thyroidectomized at the age 4, 6 or 10-12 weeks and have retained a low prolactin level similar to that in the diestrous stage of normal cycling rats thereafter. The present results suggest that regulatory system of prolactin secretion became labile by androgenization and this status led to the release of prolactin by LHRH treatment after thyroidectomy.

Luteinizing hormone-releasing hormone in peripheral plasma and hypothalamus of normal and ovariectomized rats.

Plasma and hypothalamic LHRH was measured by specific radioimmuno-assay in intact and ovariectomized rats, and the values were correlated with peripheral plasma (PP) FSH and LH titers. At most stages of the estrous cycle, plasma LHRH was either undetectable or present at very minimal values. An increase in PP LHRH concentration was observed in some animals between 13.00 and 20.00 h on proestrus. The mean elevation in LHRH was greatest in rats when blood samples were taken by decapitation; elevation was somewhat less when samples were taken from etherized rats and minimal when taken from rats bearing indwelling jugular cannulae. LHRH was elevated in approximately half the ovariectomized animals; repeated samples were drawn at 15-min intervals from intrajugular cannulae. In animals with LHRH elevations, LHRH was highly variable, which indicates that it is released in pulsatile fashion. Plasma LHRH and LH titers were correlated in ovariectomized animals. The relatively low correlation between LHRH and LH may be explained by the fact that a pulse of LHRH can elicit LH release over a considerable time span; also, LHRH is cleared much more rapidly from the circulation than is LH, as revealed by the time course of disappearance of exogenous LHRH given by bolus injection. In intact rats, hypothalamic LHRH content was slightly lower at 10.00 h on diestrus day 1 than at other sample times. LHRH was significantly lower 4 weeks following ovariectomy compared to levels in intact rats at any sample time. It would appear that LHRH's resynthesis does not keep pace with its release in ovariectomized rats, resulting in a decline in hypothalamic stores.

Influence of the estrous cycle and prostaglandins on utero-ovarian vein blood flow in the rat

The blood flow rate in the utero-ovarian vein (UOV) has been measured in adult female rats during the different phases of the estrous cycle. It was observed that the blood flow rate in the UOV is high at proestrus and at estrus and low during diestrus days 1 and 2. The intravenous injection of 10 μg PGF 2α or PGE 2 diminishes the blood flow rate in the UOV. The efficacy of the two PGs in reducing blood flow is different in the various phases of the estrous cycle, being maximal during the day of estrus.

Steroid control of gonadotropin release

Several studies have led to the concept that the length of the rat estrous cycle is dependent on the timing of estrogen (E) secretion. According to this hypothesis E secretion during the 5-day cycle is delayed. However, we have found LH and E levels in both 4 and 5 day cycles are identical. Therefore, even though E is critical for a cyclic gonadotropin release to occur it does not appear to be the factor, which under normal circumstances, determines cycle length. During the day of proestrus, progesterone (P) increase coincided, but did not precede the gonadotropin(s) surge in our study thus eliminating P as the normal physiological trigger of gonadotropin release. If P was the determining factor, one would expect to find 5-day P levels higher than 4-day cycle levels during the earlier stages of the cycle. Approximately 48 h following ovulation, on the day of diestrus, we found that the 5-day cycle did indeed have higher P levels. We propose that the regulation of P secretion during the early stages of the cycle controls the timing of the normal periodic gonadotropin release.

Alterations during the estrous cycle in the responsiveness of the pituitary to subcutaneous administration of synthetic LH-releasing hormone (LHRH).

To further evaluate the alterations in responsiveness of the pituitary to synthetic LHRH during the proestrous discharge of gonadotropins, LHRH was given SC in the hope of producing a release of FSH as well as LH, and blood samples were removed prior to and at various intervals after the injections of the neurohormone while the rats were anesthetized with tribromoethanol. The procedure of anesthesia and blood sampling produced small declines in both FSH and LH, but these only achieved significance in the case of FSH on the morning of estrus and diestrus day 2. An increase in plasma LH occurred in response to LHRH at all stages of the estrous cycle but was minimal during diestrus. The increment in plasma LH was already increased by 9 AM on proestrus and the titer remained elevated for 2 h. A further increase in response to LHRH occured at 2 PM associated with an increase in initial plasma LH. The maximum response occurred at 5 PM together with maximal initial plasma LH, and the characteristics of the response changed such that there was a much larger increase in plasma LH at 20 min and a rapid decline thereafter, so that the response became pulselike. Initial plasma LH had already declined significantly by 9 PM, and this was associated with a dimished pulselike release of LH in response to LHRH. By the morning of estrus, an even smaller pulse-like release occurred. Significant FSH release in response to LHRH occurred at all stages of the cycle as indicated by the increments in plasma FSH. The relative increase in plasma titers was much less than that for LH and responsiveness to LHRH did not increase until 5 PM on proestrus. Responsiveness had already begun to decline by 9 PM on proestrus and by the morning of estrus was similar to that obtained on diestrus. Initial plasma FSH titers were first elevated by 2 PM on proestrus and they remained elevated on the morning of estrus. The results indicate that maximal responsiveness to LHRH in terms of LH release is associated with the proestrous discharge of LH, but that the maximal responsiveness in terms of FSH release terminates long before the endogenous release of hormone ceases sometime on estrus. The increased responsiveness in terms of LH release may be related to prior estrogen secretion and to the priming action of endogenous LHRH. The continued release of FSH in the face of a return of responsiveness to LHRH to low levels indicates that release of FSH on late proestrus and early estrus is not caused by endogenous release to LHRH.

Augmentation of pituitary responsiveness to luteinizing hormone/follicle stimulating hormone-releasing factor (LH-RF) as a result of acute ovariectomy in the four-day cyclic rat.

Within 6 h of ovariectomy in adult rats with 4-day estrous cycles, plasma FSH titers were significantly elevated above those of sham-operated controls at all stages of the estrous cycle, whereas plasma LH concentrations were raised by ovariectomy only during diestrus day 2, proestrus or estrus. A single intravenous injection of a partially purified extract of ovine stalk-median eminence tissue (LH-RF) into sham-operated control rats or incubation of pituitaries from similar rats with the same releasing factor extract elevated LH and FSH output at all stages of the cycle. This response to LH-RF was related to the stage of the estrous cycle, maximal pituitary responsiveness occurring on proestrus. Ovariectomy 6 h before administration of LH-RF significantly augmented pituitary LH and FSH responsiveness both in vivo and in vitro. This elevation in hypophyseal responsiveness observed in vitro followed a cyclic pattern which could be superimposed on the normal cyclic changes in pituitary responsiveness, whereas the cyclic increase in pituitary LH responsiveness to LH-RF in vivo following acute ovariectomy was first detectable 16 to 18 h earlier than in intact controls, that is, on late diestrus day 2 rather than on the morning of proestrus. These results indicate that acute ovariectomy can augment pituitary responsiveness to LH-RF and can also advance the onset of the cyclic augmentation of pituitary responsiveness to LH-RF during the 24 h immediately preceding the ovulatory gonadotropin surge. Possible explanations for these effects are discussed.

Ovarian responses to perphenazine-induced prolactin secretion in the rats: Effect of ovulation, stress, and steroids.

A single injection of 2.5 mg perphenazine (PH)/kg body wt to rats on the day of estrus (day 0) did not result in increased serum progesterone 24 hr later. Continued daily injections, however, resulted in a 2.5-fold increase in serum progesterone between days 1 and 3 and a 1.6-fold increase between days 3 and 5 to a final concentration of 58 plus or minus 4 ng/ml on day 5 in serially anesthetized and bled rats. Neither daily administration of 5.0 nor 10.0 mg PH/kg body wt to rats subjected to the stressful conditions of this regimen resulted in further increases in serum progesterone, but the 5.0 mg dose of PH in unstressed rats bled only on day 5 resulted in a highly significant increase in serum progesterone to 110 plus or minus 7 ng/ml. In unstressed rats the increase in serum progesterone over control values after five daily injections of 2.5 mg PH/kg body wt could be attributed to decreased 20alpha-reduction of progesterone, but when the dose of PH was increased to 5.0 mg/kg, a highly significant increase in both progesterone and total progestins occurred indicating that prolactin can increase steroidogenesis as well as reduce 20alpha-hydroxysteroid dehydrogenase activity. After inhibition of ovulation, the 5.0 mg daily dose of PH resulted in serum progesterone of only 25 plus or minus 8 ng/ml on day 5 in unstressed rats. Thus, serum progesterone in ovulating rats treated with PH originated primarily in the corpora lutea. Perphenazine, 5.0 mg/kg, administered only on estrus and the first day of diestrus was sufficient to induce pseudopregnancy of 14.5 plus or minus 1.6 days. No evidence for gonadotropin stimulation of the ovaries of any rats was observed. The effect of stress on the progesterone response was not mimicked by administration of cortisol acetate and is assumed to be medicated by suppression of prolactin secretion.

Serum prolactin and LH in early phases of delayed versus direct pseudopregnancy in the rat.

Delayed or direct pseudopregnancies were induced by electrical stimulation of the cervix at 1400 h on diestrus day 2 (D-2) or on estrus, respectively. Blood samples for measurement of prolactin and LH by radioimmunoassay were collected by rapid decapitation at 5, 15, 30, 45 or 60 min after cervical stimulation or thereafter at 3-h intervals throughout the first 6 days of leukocytic vaginal smears of pseudopregnancy (PSP L-1 to L-6). For comparison, untreated animals were decapitated at the same 3-h intervals throughout the 4-day cycle. Serum LH concentrations in all the experimental animals did not vary from those measured in the cyclic controls. Compared with the normal cycle, prolactin (PRL) levels were not different until 10 h after cervical stimulation during estrus. After stimulation on D-2, PRL secretion did not differ from that in the normal cycle until approximately 37 h later, when there was a short rise following the usual proestrus surge. In both direct and delayed pseudopregnancy, twice-daily PRL surges appeared on L-1 and, except for a missing nocturnal surge on L-2 in delayed PSP, continued regularly through L-6. The absence of any immediate increase of PRL following the D-2 stimulus strongly supports the view that information from the stimulus is retained in the central nervous system to be expressed later after a set of new, competent corpora lutea has been formed.

Progestational Function of Perifused Rat Corpora Lutea

Corpora lutea (CL) from synchronously ovulated, prepubertal rats remained viable in perifusing Eagle medium (Dulbecco modified) flowing at a rate of 1 ml/hr. As an index of viability, progesterone (P) and 20alpha-hydroxypreng-4-ene-3-one (20alpha-OH-P) were determined by radioimmunoa-say in effluent media. Corpora lutea removed on the 2nd day of diestrus (D-2) or the 2nd day of pseudopregnancy (PP-2) showed fatigue by a continuous decline in the concentrations of effluent progestins. P decreased from 2 to 0.2 ng/ml/CL during an interval of 5 hr, while 20alpha-OH-P decreased from 2.2 to about 0.7 ng/ml/CL. In contrast corpora lutea taken on PP-4 maintained higher progestin levels in the effluent media. P present initially at 2.2 ng/ml/CL decreased to 0.73 ng/ml/CL; 20alpha-OH-P, initial concentration 0.84 ng/ml/CL, decreased to 0.41 ng/ml/CL. The greater functionality of PP-4 CL indicated by the continued predominance of , suggested an in vivo imposition of a luteotropic stimulus occurring after PP-2. Addition of bovine LH (NIH-LH-B8, 20 mug/ml) to the perifusing medium stimulated steroidogenesis by PP-2 CL during which 20alpha-OH-P levels remained between 2.3 and 3.2 ng/ml/CL throughout perifusion, while P secretion decreased from 2.9 to 0.9 ng/ml/CL. Prolactin (NIH-P-B3, 20 mug/ml), did not significantly alter the original secretion pattern of PP-2 CL. During combined prolactin (20 mug/ml) and LH (2 to 10 mug/ml) perifusion, P secretion predominated, decreasing from 3.9 to 1.0 ng/ml/CL; 20alpha-OH-P decreased from 1.2 to 0.7 ng/ml/CL.

Acute and chronic effects of the fornix section on cyclic gonadotropin secretion and ovulation in the rat.

The fornix was sectioned in the frontal plane by means of a razor blade knife, and acute and chronic effects of this section on gonadotropin secretion were estimated. The 5-day cyclic rat which received the section of fornix under either anesthesia at 12:00 on the day of diestrus II showed advancement of the proestrous and estrous vaginal smears and as well as ovulatory gonadotropin release by one day. It was revealed that the primary effect was the inducement of FSH release on the day of section. The 4-day cyclic rat bearing the fornix section chronically resumed vaginal cyclicity after elapsing the diestrous period for 18 to 25 days. The rat ovulated normally and mean number of ova inoviducts was not different from that in the intact rat. However, the sectioned rat hadan higher concentrations of pituitary and serum FSH on the day of diestrus II than thatin the intact rat, and had an higher concentration of serum LH on the day of estrus. These results indicate that the hippocampus exerts the inhibitory influence on LH and FSH release and if this is eliminated the facilitatory influence dominates the brain mechanism controlling gonadotropin release, resulting in the advancement of estrous cycle (the acute effect) or the increase of gonadotropin release (the chronic effect).

Localization and Mechanism of Stimulatory Feedback Action of Estrogen: Effect of Limbic Forebrain Implantation of Estradiol Benzoate on Advancement of Ovulation

The sites and mechanism of the ovulation-inducing action of estradiol benzoate (EB) were studied by brain implantation of the crystalline steroid through chronically implanted outer cannula at 12:00 on diestrus day 2 in the 5-day cyclic rat. EB implantation in the medial amygdala or the bed nucleus of stria terminalis advanced cyclic changes in vaginal smears, timing of ovulatory LH release, and ovulation by 1 day, resulting in 4-day cycle. When implants in the bed nucleus of stria terminalis were placed for a shorter period of time on diestrus day 2, from 12:00 to 20:00, advancement of these parameters were similarly observed. Serum concentration of FSH and that of prolactin were significantly elevated at 20:00 on the same day in the rats implanted with EB in the medial amygdala or the bed nucleus of stria terminalis, compared with those in the non-treated controls. LH was not affected. The implantation in the arcuate nucleus was also effective to advance ovulation, but the anterior deafferentation prevented the effect. In contrast, EB implantation in the medial septal nucleus, the medial preoptic area, or the medial basal prechiasmatic area was consistently ineffective to advance vaginal cycle and ovulation. Multiunit activity in the arcuate nucleus showed an afternoon elevation on the day of implantation in these areas and as well on the day following, while it did not show such elevation on the day of implantation in the medial preoptic area. It is concluded that EB acts on the medial amygdala and the bed nucleus of stria terminalis in the mid-diestrus in 5-day cycle to stimulate FSH and prolactin release without affecting LH, which changes trigger a chain of reproductive events inducing early release of ovarian steroid responsible for early ovulatory gonadotropin release. The arcuate nucleus in one of the sites of stimulatory action of estrogen, but it requires the neural influence presumably from the medial amygdala and the bed nucleus of stria terminalis via the preoptic area for stimulating the ovulatory hormone release. EB exposure is considered to be endowed with the increase of its responsibility to this neural influence.

Role of brain monoamines in release of gonadotropin before proestrus in the cyclic rat.

To determine whether brain monoaminergic neurons are involved in the release of gonadotropins responsible for estrogen increases before proestrus, various inhibitors and precursors of monoamine biosynthesis were administered subcutaneously or intracranially to the 3rd ventricle at 10.00 or 20.00 on the day before proestrus, the 2nd day of diestrus (DII) in 4-day cycling rats. The inhibitors used were alpha-methyl-p-tyrosine (alpha-MPT) and bis-(4-methyl-1-homopiperazinyl-thiocarbonyl)-disulfide (FLA-63). The effects of these drugs on changes in vaginal cytology, ovulation, uterine weight of uterine intraluminal fluid, and on serum concentrations of LH and FSH were evaluated in selected experiments. (1) Administration of alpha-MPT (150 mg/kg s.c.), an inhibitor of tyrosine hydroxylase, at 10.00 on DII reduced weights of uterus and intraluminal fluid on the day of expected proestrus (P), prevented vaginal cornification on estrus (E), blocked ovulation in all 10 rats, and induced prolonged diestrus. (2) Administration of FLA-63 (10 mg/kg s.c.), an inhibitor of dopamine-beta-hydroxylase, at 10.00 on DII reduced weights of uterus and intraluminal fluid on P, blocked ovulation for a few days but did not prevent vaginal cornification at the expected time of E. (3) Administration of alpha-MPT (200 mg/kg) or FLA-63 (15 mg/kg) at 20.00 on DII blocked ovulation in all of 8 and 7 rats, respectively, but these treatments did not block vaginal cornification at the expected time in any animal. (4) Administration of L-DOPA (100 mg/kg) or dihydroxy-phenylserine (DOPS, 200 mg/kg) with alpha-MPT (200 mg/kg) at 20.00 on DII reversed the blocking effect of alpha-MPT on ovulation in 3 out of 6 and 3 out of 5 rats, respectively. (5) Direct application of crystalline alpha-MPT or FLA-63 (about 3-5 mug) to the 3rd ventricle at 20.00 on DII also blocked ovulation in all of 7 and 5 rats, respectively. (6) Both systemic and intraventricular injections of alpha-MPT at 10.00 on DII reduced serum LH on P but not serum FSH. FLA-63 by intraventricular injection also reduced serum LH but not serum FSH. (7) Injection of 17beta-estradiol (40 mug s.c.) with alpha-MPT or FLA-63 partially removed the ovulatory blockade induced by conditions 1, 2, 3 and 5. Therefore, norepinephrine seems to be an important neurotransmitter in the release of gonadotropin responsible for estrogen secretion before P, but dopamine may also be involved during its early stage as represented by 10.00 on DII.

Effects of estrogen on neuronal excitability in the hippocampal-septal-hypothalamic system.

The effects of electrical stimulation of the medial preoptic area (MPO) upon unit firing in the periventricular arcuate nucleus, and that of the dorsal hippocampus (DHPC) on medial septo-preoptic and arcuate (ARC) neurons, were investigated in Wistar and Sprague-Dawley female rats throughout the 4-day estrous cycle. Unit activity was recorded using stereotaxically-oriented tungsten microelectrodes under light urethane anesthesia. Repetitive stimulation of monophasic square waves varying only in current intensity was used. The following results were obtained: (a) An increase in activity of all ARC neurons recorded was induced by MPO stimulation on each day of the estrous cycle. (b) The minimum current (threshold) effective in increasing activity in the ARC neurons varied throughout the estrous cycle; the lowest threshold was observed in proestrus and the highest on the first day of diestrus. Also, the threshold current of MPO stimulation required in increase ARC activity was found to be elevated after ovariectomy and markedly reduced to the levels of the proestrous animal by estrogen treatment. (c) Stimulation of the DHPC (field CA3) increased activity in the medial septum but decreased activity in the MPO. Two pools of neurons, one increased and one decreased by DHPC stimulation, were observed in the ARC. (d) Variation in the threshold hippocampal stimulation during the estrous cycle was observed in the response of MPO and ARC neurons (the stimulation was effective only in proestrus and estrus); but not in that of medial septal neurons. (e) In addition, the spontaneous activity of septal; MPO; and ARC neurons was increased at proestrus or after estrogen injection. The present results suggest that plasma levels of estrogen play an essential role in the cyclic process of the regulation of ovulation by way of the selective facilitation of neuronal excitability in specific functional neural pathways. Furthermore, the results support the existence of a hippocampal inhibitory projection originating in field CA3 and terminating in the final common pathway, MPO to ARC.

Possible role of anterior inputs to the medial basal hypothalamus (MBH) in regulating prolactin release during pseudopregnancy in the rat

The effects of transection of fiber connections with the medial basal hypothalamus (MBH) on induction or maintenance of pseudopregnancy (PSP) were studied. PSP was induced ‘pharmacologically’ by injecting reserpine (1 mg/kg) on the day of diestrus I in 4-day cycling rats or the corresponding day after induction of ovulation in persistent estrous animals. Postero-bilateral deafferentation (PBLD) which cuts dorsal, lateral and posterior connections to the MBH failed to influence the induction of PSP. All rats resulted in PSP following reserpine injection. Anterior deafferentation (AD) which interrupts the preoptic-hypothalamic connections induced anovulatory persistent vaginal estrus. In these AD rats, reserpine could not activate new corpora lutea which had been formed by a pretreatment with 10 I.U. HCG. However, replacement therapy with 20 I.U. prolactin was successful in activating these corpora lutea. In spite of the AD, all rats thereafter remained in diestrus, massive deciduomata being formed following uterine trauma. In the second series of experiments, the AD or roof deafferentation (RD) was performed 3 days after reserpine injection. The AD effectively interrupted reserpine-induced PSP. However, this effect of the AD was reversed by the replacement with prolactin from the day of operation. PSP was also not interrupted by the AD when reserpine was given supplementarily from the day of the AD through the day before autopsy, but a single dose of reserpine only on the day of the AD was not effective in maintaining PSP in AD rats. The RD which removes dorsal afferents to the preoptic area (POA) and hypothalamus did not interfere with PSP; it continued in all rats of the group. These results suggest that neural influence originating from the POA or more rostral regions is necessary to maintain prolonged release of prolactin during PSP. Since successive injections of reserpine were needed to keep the AD rats pseudopregnant, reserpine sensitive neural structures which may locate behind the surgical cut seem to be unable to support independently prolonged release of prolactin during PSP.

Influence of the estrous cycle and prostaglandins on utero-ovarian vein blood flow in the rat

The blood flow rate in the utero-ovarian vein (UOV) has been measured in adult female rats during the different phases of the estrous cycle. It was observed that the blood flow rate in the UOV is high at proestrus and at estrus and low during diestrus days 1 and 2. The intravenous injection of 10 μg PGF 2α or PGE 2 diminishes the blood flow rate in the UOV. The efficacy of the two PGs in reducing blood flow is different in the various phases of the estrous cycle, being maximal during the day of estrus.

Cyclic activity of estrogen sulfotransferase in the gilt uterus.

Minced uteri from gilts in various days of the estrous cycle were incubated for 2 hr with l7β-estradiol-6,7-3H, (∼5 × 10−9M) and Na2 35SO4 (∼ l × 10−4M), and sections of the same uterine horns and the corresponding ovaries were prepared for histological examinations. When the estrogens were extracted from the incubation and separated into unconjugated and sulfated fractions, it was found that sulfation varied with the day of the cycle. At estrus and in the immature animal there was no sulfation of estrogens. Estrogen sulfotransferase activity began to appear at metestrus (day 3) and at diestrus (day 6) rose sharply to a peak level around day 9 (80% of the labeled estrogen sulfated). Although the unconjugated fraction contained predominantly 17β-estradiol, most of the conjugated fraction consisted of estrone sulfate. Incubations carried out for various time intervals revealed a constant rate of sulfation of estrogens, previously formed estrone being the favored substrate. The proportion of the sulfate frac...

Biphasic effect of estradiol benzoate on the pituitary responsiveness to LH-RH.

Pituitary responses to LH-releasing hormone (LH-RH) was studied in normal diestrous rats 2, 4, 6, 9, 14, 24, and 48 hr after injection of estradiol benzoate (EB). A dose of 0.4 µg LH-RH always raised serum LH in the oil-treated rats. The magnitude of the increase varied according to the stage of the estrous cycle, being greatest in proestrus, and smallest between the evening of the day of diestrus I and the morning of the day of diestrus II. Two to 6 hr after pretreatment with EB, injection of this dose of LH-RH failed to induce a significant rise of serum LH. At 9 hr, the same dose of LH-RH did increase serum LH, the magnitude of the response being the same as that found in the oil-treated control rats. By 14–24 hr, EB had augmented the pituitary response to LH-RH. At 48 hr, the magnitude of the rise of serum LH after LH-RH in EB-treated rats was like that found at 24 hr, but this high responsiveness to LH-RH apparently can not be attributed to the EB since a similar responsiveness was seen in the respec...