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N Parvizi

Publications and source records attributed to N Parvizi.

At least 37 records · Page 2Linked to original sources

Ovarian modulation of the oestradiol-induced LH surge in prepubertal and sexually mature gilts.

The role of ovarian secretions in modulating positive oestrogen feedback on LH release in late prepubertal and sexually mature gilts was studied. Gilts were either ovariectomized (OVX) at 230 days of age (sexually mature, OVX 230, control), ovariectomized at 160 days of age (pre-pubertal, OVX 160) or ovariectomized at 160 days of age and given either low, high or very high oestradiol substitution therapy (two or three Silastic implants, 5 or 8 cm in length) from 160 days to 230 days (OVX 160 + 2E5, OVX 160 + 2E8 and OVX 160 + 3E8, respectively). The LH surge responses to three i.m. injections of oestradiol benzoate given at intervals of 12 h (in total 10 micrograms oestradiol benzoate kg-1 bodyweight) were compared at 260 days. An additional group of sexually mature gilts was ovariectomized at 260 days (OVX 260) and challenged with oestradiol benzoate at 360 days. LH surges with peak LH concentrations below pretreatment values (resembling LH responses to oestradiol benzoate in immature gilts) were classified as immature, and those with peak LH concentrations above pretreatment values as mature. LH concentrations before treatment with oestradiol benzoate were reduced (P < 0.05) in OVX 160 + 2E8 and OVX 160 + 3E8 gilts compared with OVX 230 (control). When compared with the control group, the time to LH surge peak was longer in OVX 260 gilts, LH peak amplitude was reduced in the OVX 160 group and the area under the curve of the LH surge (ng LH ml-1 plasma (48 h)-1) was less in all other groups (P < 0.05). Classification of LH surges by mature:immature criteria indicated a high mature:immature ratio in OVX 230 gilts (6/1) and a low ratio in OVX 160 (1/7) and OVX 260 (1/6) gilts. The long-term effect of ovariectomy was partially overcome in the OVX 160 + 2E5 group (mature:immature = 3/3). However, previous exposure to supraphysiological concentrations of oestradiol (as in groups OVX 160 + 2E8 and OVX 160 + 3E8) resulted in a high percentage of animals (66% and 100%, respectively) that did not respond to the oestradiol benzoate challenge with an LH surge. Immediately before oestradiol benzoate administration (30 days after removal of implants) plasma oestradiol concentrations in these two groups were still high (P < 0.05) compared with all other groups. GnRH-induced (0.2 microgram kg-1 bodyweight) LH secretion, evaluated 10 days after treatment with oestradiol benzoate, was depressed (P < 0.05) in OVX 160 + 3E8 gilts, but not affected by age at ovariectomy. We suggest that continuous ovarian secretion is necessary for the final maturation of the LH surge mechanism in late prepubertal gilts and also for maintaining the full functionality of this mechanism in sexually mature gilts. The range over which ovarian oestrogens tune the final maturation of this process appears to be rather narrow; however, other ovarian factors may contribute to the final maturation. Furthermore, continued exposure to supraphysiological concentrations of oestradiol was found to be detrimental to the development of the LH surge mechanism.

Analysis of Variance↗

LH profile and advancement of ovulation after transcervical infusion of seminal plasma at different stages of oestrus in gilts.

The influence of a transcervical infusion of seminal plasma on preovulatory LH profiles and the advancement of ovulation after seminal plasma infusion for different times during oestrus were investigated using the single uterine horn infusion technique (Mariensee model), in combination with transcutaneous sonographic monitoring of the ovaries. Preparative surgery in 23 German Landrace gilts comprised the detachment of the left uterine horn from the corpus, leaving the caudal end open to the peritoneal cavity but sealing the corpus wound. In six gilts fitted with a permanent jugular vein catheter the patent horns were administered a transcervical infusion of seminal plasma (n = 5 cycles) or PBS (n = 4 cycles) immediately after the detection of oestrus by a teaser boar. In addition, 17 non-catheterized gilts received infusions of seminal plasma either 0 h (n = 3 gilts), 16 h (n = 7 gilts) or 24 h (n = 7 gilts) after the detection of oestrus. Seminal plasma infusion at the onset of oestrus provoked ovulation in the ipsilateral ovary of the treated horn 8.5 +/- 0.9 h earlier than in the contralateral (control) ovary. Seminal plasma did not influence the LH profile compared with PBS (P > 0.05), but shortened the interval between the LH peak and ipsilateral ovulation to 23.4 +/- 4.0 h compared with 31.8 +/- 3.4 h in the contralateral ovulation (P < or = 0.01). Infusion 16 h after the onset of oestrus reduced the effect to 4.6 +/- 3.8 h with a wide range of 0-8 h (P < 0.01). The effect was more pronounced in gilts with long intervals between the onset of oestrus and contralateral ovulation compared with earlier ovulation on the control ovary. Seminal plasma infusion less than 16 h before contralateral ovulation and 24 h after the detection of oestrus had no effect. It is concluded that transcervical infusion of seminal plasma early in oestrus synchronizes the variable intervals between the onset of oestrus and ovulation in sows by a locally active mechanism.

Animals↗

Pulsatile and diurnal secretion of GH and IGF-I in the chronically catheterized pig fetus.

The ontogeny of GH and IGF-I secretion was investigated in the fetal pig. Pulse studies were performed to describe the pattern of GH release. Twenty-four-hour profiles were recorded to examine possible diurnal variations in these hormones. (I) PULSE STUDIES: Blood samples were obtained at 15-min intervals for 2-h periods from 24 male and 20 female fetuses at various gestational ages (fetal day 89-113; term 113 +/- 1 S.D.). Fetuses revealed a pulsatile GH release. The GH pulse frequency did not vary with gestational age in either sex (0.95 +/- 0.19 pulses/h). In males the GH pulse amplitude decreased with increasing fetal age (r = -0.41; P < 0.02). In female fetuses no significant correlation could be calculated. Mean GH concentrations fell significantly in male fetuses 3 to 4 days before delivery (P < 0.05) and the same tendency was observed in females (P < 0.06). Between fetal days 94 and 98 GH pulse amplitude and GH and IGF-I concentrations were higher in males than in females (P < 0.01, P < 0.001 and P < 0.02 respectively). Fetal IGF-I secretion showed no ontogenetic changes in both sexes. However, maternal IGF-I concentrations increased with progressing gestation (r = 0.46; P < 0.001). (II) 24-H PROFILES: Eight male and four female late-gestational fetuses (fetal days 104-108) were studied. Blood samples were taken at 30-min intervals over 24 h. Dams and fetuses showed an episodic GH secretion over the 24-h period but no diurnal rhythm was observed. Whereas maternal IGF-I secretion was constant, fetal IGF-I release was characterized by marked fluctuations over the 24 h. In half of the fetuses (n = 6) the fluctuations appeared at regular intervals. Again no diurnal rhythm existed. These data demonstrated that: (1) porcine fetal GH secretion is pulsatile and decreases shortly before birth; (2) a sex difference in GH and IGF-I concentrations exists between fetal days 94 and 98, suggesting that IGF-I is at least partially under the control of GH before birth; (3) fetal GH and IGF-I secretion is episodic over 24 h, but does not vary diurnally; and (4) fetal and maternal GH and IGF-I secretion are regulated independently.

Animals↗

Effect of naloxone and pulsatile luteinizing-hormone-releasing hormone infusions on oestradiol-induced luteinizing hormone surges in immature gilts.

The aim of the study was to understand why immature 60-day-old gilts produce delayed low amplitude luteinizing hormone (LH) surges in response to oestradiol benzoate. In Expt 1, gilts (n = 36) were challenged with oestradiol benzoate and subsequently received either no further treatment or were infused with saline or various doses of the opioid antagonist, naloxone, for 6-48 h during the expected LH surge (48-96 h after oestradiol benzoate). No differences were observed among groups in the magnitude or duration of the LH surge. In contrast to the other groups, LH concentrations in gilts infused for 48 h with naloxone did not decrease after the surge period. In Expt 2, gilts (n = 34) were challenged with oestradiol benzoate or sesame oil and subsequently received pulses of luteinizing-hormone-releasing hormone (LHRH) or saline solution during the expected surge period. Two other groups were fed methallibure to pharmacologically suppress the oestradiol benzoate-induced LH surge. In addition, one of these groups was given pulses of an LHRH agonist (LHRH-A) during the surge period. Within 2 h of the start of pulsatile LHRH infusion, LH increased in sesame oil-treated gilts, but not in oestradiol benzoate-treated gilts, suggesting that the pituitary responsiveness to LHRH in immature gilts is decreased by oestrogen before the onset of the LH surge. Pulsatile LHRH infusion did not enhance the amplitude of oestradiol benzoate-induced LH surges nor did it advance its onset. Feeding methallibure suppressed the oestradiol benzoate-induced LH surge.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Beta-endorphin in sows during late pregnancy: effects of cloprostenol and oxytocin on plasma concentrations of beta-endorphin in the jugular and uterine veins.

Beta-endorphin was measured in the plasma of pigs during late pregnancy and at different stages of the oestrous cycle. In pregnant animals, beta-endorphin secretion from uteroplacental tissues into the maternal circulation and the possible effects of oxytocin and the prostaglandin F2 alpha (PGF2 alpha) analogue cloprostenol on beta-endorphin release were determined. Plasma beta-endorphin concentrations in pregnant sows were significantly higher than in non-pregnant pigs. However, there were no significant changes in beta-endorphin values throughout the oestrous cycle. Because the increase in plasma beta-endorphin concentrations had occurred before luteolysis and onset of labour it could not be attributed to the stress of parturition. The surgical intervention of a laparotomy increased beta-endorphin release into peripheral plasma. Cloprostenol but not oxytocin caused an immediate increase in plasma beta-endorphin concentrations. At parturition, endogenous PGF2 alpha may be involved in the regulation of beta-endorphin secretion. Concentrations of beta-endorphin in the jugular and uterine vein plasma were not significantly different, and so it would appear that beta-endorphin in the plasma of pregnant sows is not of uteroplacental origin. In conclusion, changes in the concentration of beta-endorphin in peripheral plasma, associated with pregnancy but not the oestrous cycle, exist in pigs. Hence a physiological function of peripheral opioid peptides in the periparturient sow is feasible.

Animals↗

Oestrus and LH responses to oestradiol during lactational anoestrus in Chinese Meishan and large white sows.

To investigate endocrine mechanisms associated with the occasional occurrence of fertile oestrus during lactation in the high prolific Chinese Meishan (MS) breed, the incidence of oestrus and changes in plasma luteinizing hormone (LH) levels before and after oestradiol benzoate (OB, 15 micrograms/kg body weight) administration on day 22 was compared in 4 MS and 6 Large White (LW) sows. All sows exhibited oestrus in response to OB. Only 1 sow (MS) ovulated in response to OB, became pregnant and farrowed. Mean plasma LH levels before OB were low (MS: 0.38 +/- 0.06 ng LH/ml, LW: 0.29 +/- 0.04 ng LH/ml, ns). LH levels above 2 ng/ml (surge) occurred in 2/4 MS and 2/6 LW sows at 60 +/- 5 h after OB. The MS sow that ovulated had an LH surge level of 4.5 ng/ml plasma at 40 h after OB. These results indicate minor breed differences in the control of LH secretion during lactational anoestrus.

Anestrus↗

Control of the LH surge mechanism in the female pig.

The functionality of the oestrogen-positive feedback mechanism is the basis for the preovulatory LH surge and thus for regular cyclic activity in the sow. The LH surge mechanism (LH SM) gradually matures as a function of age, immature gilts display delayed, low amplitude LH surges in response to oestradiol benzoate (OB). The maturation of the LH SM apparently is ovarian oestrogen-dependent. Continuous ovarian secretions, probably oestrogens, also appear to be necessary for the final peripubertal maturation of the LH SM and to maintain the functionality of this mechanism in the sexually mature gilt. Superphysiological levels of oestrogens are, however, detrimental to the development of the LH SM. Failure of various infusions of the opioid antagonist naloxone during the surge period to enhance the magnitude of OB-induced LH surges in immature gilts does not support the idea, that central opioidergic systems are of major importance in preventing mature LH surge response at this age. However, opioids could be involved in the termination of the LH surge. Experiments using the opioid agonist morphine and the antagonist naloxone to demonstrate that opioids are involved in the generation of the LH surge in the mature gilt have so far provided equivocal data. Studies using pulsatile infusions of LHRH or of a potent LHRH-agonist during the surge period in OB-treated immature gilts, in which endogenous LHRH release was blocked by methallibure, suggest that oestradiol fails to generate mature LH surges because the gonadotrophs of the immature gilt are unable to respond to enhanced LHRH secretion during the surge period in an adult-like manner. During early lactation the LH SM cannot be activated by OB, while during late lactation a partial recovery of the LH SM occurs. Minor breed differences exist in the functionality of the LH SM during lactation between LW sows and highly fertile Chinese Meishan sows, in which lactational anoestrus is not obligatory.

Age Factors↗

Opioid binding in the rostral hypothalamus is reduced following lesion of the ventral noradrenergic tract in female rats.

Experiments were undertaken to establish whether opioid receptors exert a direct presynaptic influence on noradrenergic (NA) terminals in the preoptic/anterior hypothalamus (PO/AH) of the female rat. Thus, opioid binding studies were performed in rats with lesions of the ventral NA tract (VNAT; the main NA projection to the hypothalamus) to assess whether a loss of NA terminals may also result in a decrease in opioid binding in the PO/AH. In the first experiment, unilateral electrolytic lesions of the VNAT caused a significant reduction in both the NA content and specific [3H]-diprenorphine binding to membrane homogenates in the ipsilateral PO/AH. In the second experiment bilateral 6-hydroxydopamine (6-OHDA)-induced lesions of the VNAT caused a significant reduction in NA levels in the PO/AH as well as significant decreases in the density of [3H]-diprenorphine binding to tissue sections of the PO/AH when compared to control animals. These results strongly suggest that the NA input to the PO/AH is regulated by endogenous opioid peptides, and provide an anatomical substrate to explain opioid-NA interactions in the control of gonadotrophin releasing hormone (GnRH) and gonadotrophin secretion.

Animals↗

Superovulation of dairy cows with purified FSH supplemented with defined amounts of LH.

This study investigated the effects of a purified follicle stimulating hormone (FSH) preparation supplemented with three different amounts of bovine luteinizing hormone (bLH) and a commercially available FSH with a high LH contamination on superovulatory response, plasma LH and milk progesterone levels in dairy cows. A total of 112 lactating Holstein-Friesian crossbred dairy cows were used for these experiments; the cows were randomly assigned to treatment groups consisting of purified porcine FSH (pFSH) supplemented with bLH. Group 1 was given 0.052 IU LH/40 mg armour units (AU) FSH (n = 6); Group 2 was given 0.069 IU LH (n = 32); Group 3 received 0.423 IU LH (n = 34); while Group 4 cows (n = 36) were superovulated with a commercially available FSH-P. This compound appeared to contain 8.5 IU LH/40 mg AU FSH according to bioassay measurement. All animals received a total of 40 mg AU FSH at a constant dose twice daily over a 4-d period. Levels of milk progesterone and plasma LH were determined during the course of superovulatory treatment. The Group 1 treatment did not reveal multiple follicular growth, and no embryos were obtained. Superovulation of Group 3 cows resulted in significantly (P<0.05) more corpora lutea (CL; 12.6+/-1.1) and fertilized ova (5.1+/-1.3) compared with Groups 2 and 4 (10.1+/-0.9 and 2.6+/-0.6, 9.0+/-0.9 and 2.7+/-0.5, respectively). Due to a high percentage of degenerated embryos (33%) Group 3 yielded only one more transferable embryo than Groups 2 and 4. Among groups, LH levels differed in the period prior to induction of luteolysis and were similar thereafter. The progesterone pattern following FSH/LH administration reflected the amount of LH supplementation. Milk progesterone levels on the day prior to embryo collection were correlated to the number of CLs and recovered embryos. It is concluded that under the conditions of our experiment superovulation with 0.423 IU LH/40 mg AU FSH may yield a significantly improved superovulatory response in dairy cows. It is further suggested that LH supplementation exerts its effects mainly on follicular and oocyte maturation during the period prior to luteolysis.

Journal Article↗

Opioid action on luteinizing hormone secretion in newborn pigs: paradoxical effect of naloxone.

German Landrace piglets, 6-7 days of age, received either saline (9 males, 8 females), 0.5 mg naloxone/kg body weight (7 males, 7 females), 2.0 mg naloxone/kg (7 males, 8 females) or 0.5 mg DADLE (potent leu-enkephalin analog)/kg (7 males, 7 females) through a catheter inserted into the jugular vein 2-4 days previously. Male or female piglets were allocated randomly, within litter, to the different experimental groups. Blood samples were withdrawn for a period of 240 min at 10-min intervals for the first 60 min following injection and at 20-min intervals for the rest of the test period. Piglets were separated from their mother via a detachable wall and were allowed to suckle every 50 min. DADLE failed to alter plasma levels of LH in both males and females. Naloxone induced a significant (P less than 0.01) decrease in LH concentrations in females 10 to 60 min after injection (saline: 2.3 +/- 0.2 ng/ml plasma (SEM); 0.5 mg naloxone/kg: 1.0 +/- 0.2 ng/ml plasma and 2 mg naloxone/kg 1.2 +/- 0.4 ng/ml plasma). In males low doses of naloxone reduced plasma LH levels 10 to 40 min after injection (saline: 2.0 +/- 0.3 ng/ml plasma and 0.5 ng naloxone/kg: 1.1 +/- 0.3 ng/ml), whereas a decrease in plasma LH levels occurred 80 to 140 min after injection of high doses of naloxone (saline: 2.1 +/- 0.2 ng/ml and 2 mg naloxone/kg: 1.0 +/- 0.2 ng/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

In vitro characterization of secretion rates from silastic micropellets containing estradiol.

For local, controlled steroid hormone administration into tissues, such as the brain, we have prepared cylindric micropellets of 1 mm in length and 1 mm diameter. The micropellets are a mixture of silicone glue (silastic) and 0.1%, 1.0%, or 10% estradiol (E2). To evaluate in vivo E2 secretion rates, micropellets were implanted into the brains of 40 rats for either 1, 4, 8, or 12 weeks. In vitro 24 h E2 secretion rates of these implants were compared-after removal from the rat brain-with 24 h secretion rates of micropellets that had been incubated for the same periods of time in vitro only. In vitro release of E2 decreased steadily but asymptotically from the first day of incubation to the 3rd or 4th week, when an apparent steady state is achieved. With any E2 concentration the coefficient of variation for 24 h release rates rarely exceeded 15% within a group. The release rates increased nonlinearly with the concentration of E2 in the pellet. Subsequent to in vivo implantation the in vitro secretion of E2 was slightly higher than the in vitro secretion of micropellets incubated for the same period of time in vitro. Thus (1) the secretion rate from a pellet can be predicted rather exactly by the mixing ratio of silastic and E2 and (2) the secretion rate from the micropellet in vitro and in vivo appears to be rather similar. It is concluded that the method described is very useful for short-term (days) or long-term (weeks, albeit not constant) local exposure of defined tissues to steroid hormones.

Animals↗

Ontogeny of pituitary gonadotrophin secretion in the fetal and post-natal pig in response to LHRH in vitro.

Monolayer cultures of anterior pituitary cells from male or female pigs of 60, 80, 105 days of fetal life or of 60, 160 and 250 days of post-natal life were prepared and treated with LHRH (1 pM to 10 nM). Dose-related increases of LH were first seen at 80 days of gestation in both sexes, while only female fetuses responded to maximal LHRH at 60 days. Basal and stimulated LH release doubled in cultures from 105-day-old fetuses when compared with those at 80 days. Compared to late fetal stages LH release was 20- to 30-fold higher in cell cultures from 60-day-old (post-natal) donors without further change during the post-natal period. In all pre- and post-natal age groups basal and maximal LH release of pituitary cells from males was lower than that of females. FSH stimulation started in male and female cells at 80 days of gestation only at LHRH concentrations exceeding or equal to 0.1 nM. By 105 days FSH secretion was dose-related and pituitary cells of females responded with higher FSH values than did those of males. In general, post-natal cells released much higher amounts of FSH than did prenatal cells. Basal and maximal release of FSH decreased during post-natal development in both sexes. Basal as well as maximal FSH release of cultures from female donors was higher than that found in cultures from male donors. Determination of total LH and FSH content in fetal pituitary cell cultures indicated that the developmental increase in gonadotrophin release potential is a function of the total gonadotrophin content in vitro. We conclude that (1) the in-vitro release of gonadotrophins to LHRH is dose-, age- and sex-dependent; (2) in the female fetal pig LH responsiveness develops earlier than FSH responsiveness; (3) apparently, these maturational changes mainly reflect alterations in pituitary gonadotrophin content; and (4) there is no simple relationship between in-vitro release and circulating gonadotrophins.

Animals↗

[Endogenous opioids and their effects on reproduction] effects].

This minireview is a short survey of regulatory actions of endogenous opioid peptides on gonadotropin secretion in sheep, pig and cattle. Particular attention is paid to the stress induced changes in endogenous opioid levels and consequent effects on reproductive functions.

Animals↗

Ontogenetic development of proenkephalin A and proenkephalin B messenger RNA in fetal pigs.

Using solution hybridization analysis and Northern blotting with complementary RNA probes labelled to high specific activity, levels of proenkephalin A and B mRNA were analyzed throughout prenatal development in the hippocampus and striatum of fetal pigs. A differential time course for the appearance of these opioid precursor mRNAs was observed: in hippocampus, both mRNAs increased linearly throughout development with proenkephalin B mRNA increasing faster than proenkephalin A mRNA. In striatum, both mRNAs behaved similarly, increasing to a maximum level around mid-gestation and declining thereafter. The differences might be attributed to differential localization of the two precursor systems in the tissues and might be of functional relevance.

Animals↗

Ontogeny of secretory patterns of LH release and effects of gonadectomy in the chronically catheterized pig fetus and neonate.

Two experiments were conducted to determine the ontogeny of secretory patterns of luteinizing hormone (LH) release and effects of gonadectomy on the characteristics of LH secretion in the chronically catheterized pig fetus and neonate. To study secretory patterns in intact animals, blood samples were collected from 44 pig fetuses and their mothers (Days 81, 99, 109 and 113 of gestation) as well as from 25 neonates (Days 4 and 8) every 15 min for 3 h (2 h on Day 81). The results indicate that the fetal adenohypophysis secretes occasional pulses of LH as early as Day 81 of fetal life. Fetal and maternal mean LH levels are low (0.25-0.50 ng/ml) at all gestational ages, with lowest values just before birth (Day 113 post coitum). Four-day-old neonates show a significant increase in pulse frequency (male and female) as well as pulse amplitude (female), relative to fetal values, leading to significant augmentations in mean LH levels. This is associated with reductions in both 17 beta-estradiol and progesterone. By 8 days of age significant sex differences in mean LH levels (males greater than females) appear. Testosterone/5 alpha-dihydrotestosterone levels (males) are low prenatally but are significantly increased after birth, possibly due to the stimulating effects of increasing LH levels. To study the gonadal control of LH secretion, forty-one 105-day-old fetuses and thirty-eight 4-day-old neonates were chronically catheterized and were either gonadectomized or remained as sham or control animals. Forty-eight and 96 h after surgery, blood samples were taken every 15 min for 3 h. No significant changes are detectable at 96 h in mean LH, pulse frequency and amplitude in female or male fetuses or in neonates. While significant reductions in testosterone levels are observed at 96 h in the male fetus and neonate, progesterone concentration is reduced only in the neonate. In the castrated female, on the other hand, neither fetus nor neonate display significant changes in circulating levels of progesterone and 17 beta-estradiol at 96 h. It is concluded that the pituitary of the pig is able to discharge LH with occasional pulses as early as Day 81 of fetal life; however, the pituitary remains suppressed until after birth, probably due to high circulating nongonadal steroids in the fetal compartment.

Animals↗

Differential effects of catecholoestradiol-17 beta and oestradiol-17 beta on concentrations of plasma LH in the fetal pig.

The effects of 2-hydroxyoestradiol-17 beta and oestradiol-17 beta on the concentration of serum LH was studied in fetal pigs. 2-Hydroxyoestradiol-17 beta (5 micrograms/fetus; n = 6), oestradiol-17 beta (5 micrograms/fetus; n = 7) or vehicle (n = 6) were injected i.v. into chronically catheterized fetal pigs at gestational ages of 105-108 days. Seven additional fetuses at the same age served as untreated controls. 2-Hydroxyoestradiol-17 beta but not oestradiol-17 beta resulted in a rapid decline in plasma LH levels from 0.82 +/- 0.21 (S.E.M.) to 0.21 +/- 0.05 micrograms/l within 20 min of injection. Baseline concentrations of plasma LH in the mothers were low (0.72 +/- 0.2 microgram/l) and were not affected by catecholoestrogen or oestrogen treatment of fetuses. The results suggest that catecholoestrogens do not modulate LH secretion in fetal pigs through an oestrogenic action. It is possible that they act by modifying catecholamine metabolism or neurotransmission.

Animals↗