Biomedical subjects

J J Swarts

Publications and source records attributed to J J Swarts.

14 recordsLinked to original sources

PubMed1997

Inhibition of the LH surge in cyclic rats by stress is not mediated by opioids.

The effects of intravenous (iv) administration of the opioid antagonists naloxone and naltrexone on the restraint-induced suppression of the pro-estrous LH surge were studied in cyclic female rats. To minimize stress during repeated blood sampling, the rats were provided with a jugular vein cannula. Restraint stress for 6 hrs starting at t = -1 h (the onset of the LH surge being at t = 0 h) caused a suppression of LH levels (including peak height) during the period of the LH surge. Repeated naloxone injections, given 3 h (1 mg), 4 h (0.5 mg) and 5 h (0.5 mg) after the onset of the LH surge, did not affect the restraint-induced inhibition neither did pretreatment with 1 mg naloxone at t = -75 min (i.e. 15 min before application of restraint). Naltrexone (2 mg) administered at t = -15 min induced higher plasma LH levels at t = -6 min. When rats were subsequently subjected to restraint for 5 hrs starting at t = -5 min, the restraint-induced inhibition of surge levels of LH was not affected. The results indicate that withdrawal of opioid activity in cyclic female rats before the presumed onset of the LH surge results in a premature rise of LH levels. This is in accordance with the notion that LH levels prior to the surge are under tonic inhibition of endogenous opioid peptides (EOP). In addition, the data show that opioid receptor antagonism during or before application of restraint does not alter the restraint-induced suppression of the LH surge. It is therefore concluded that EOP do not mediate the inhibitory effect of restraint stress on the LH surge in cyclic rats.

Animals↗

PubMed1996

Effect of CRH on the preovulatory LH and FSH surge in the cyclic rat: a role for arginine vasopressin?

The effect of intracerebroventricular (i.c.v.) injection or infusion of various doses of corticotropin-releasing hormone (CRH) on the LH and FSH surge was studied in pro-oestrous rats supplied with a jugular vein and an i.c.v. cannula. Additionally, we investigated if arginine vasopressin (AVP) was involved in the CRH-induced alterations to the surge of gonadotropins. I.c.v. injection of 10 micrograms CRH given 5 min before the presumed onset of the LH surge caused a strong inhibition of the LH surge and a slight inhibition of the FSH surge. Three to four h after CRH injection, its inhibitory effect diminished. A 6'h i.c.v. infusion of CRH started 1 h before the presumed onset of the LH surge, caused a dose-related inhibition of the LH and FSH surge. Infusion of 1 micrograms/h CRH did not suppress the surge of both hormones while infusion of 5 or 10 micrograms/h CRH inhibited the LH surge. Infusion of 10 micrograms/h CRH caused a strong suppression of plasma LH during the first 3 h of the LH surge. Despite continuation of CRH infusion, the inhibitory effect disappeared and plasma LH increased to similar levels as in controls at corresponding points of time of the LH surge. The FSH surge was also suppressed by infusion of 10 micrograms/h CRH. The surge of LH and FSH was not affected by a 9-h infusion of 10 micrograms/h CRH started 4 h before the presumed onset of the LH surge. This observation also indicates that the inhibitory effect of CRH may last for only 3-4 h. The surge of LH and FSH was not affected by i.c.v. injections of AVP-antiserum. However, pretreatment with AVP-antiserum prolonged the inhibitory effect of CRH on the LH surge. In conclusion, CRH can inhibit the pro-oestrous LH and to a lesser extent the FSH rise for only 3-4 h after the beginning of CRH administration. AVP may play a role in limiting the inhibitory effect of CRH on LH to 3-4 h.

Animals↗

PubMed1995

Luteolytic and antiluteolytic effect of the antiprogestagen RU486 in pseudopregnant rats.

To study the effects of the antiprogestagen RU486 on luteal activity in pseudopregnant rats, adult female rats made pseudopregnant by sterile copulation were given daily injections with oil vehicle or with RU486 (2 mg/day) either during the entire period of pseudopregnancy (day 1 till day 14) or during the second half of pseudopregnancy (day 8 till day 14). Blood was taken every other day to measure serum concentrations of progesterone. At autopsy, on day 15, the weights of ovaries, isolated corpora lutea and pituitary glands were recorded. In a second study using the same experimental protocol, blood was taken via a jugular vein cannula on days 8, 9, 10 and 11 after induction of pseudopregnancy; on each of these days blood samples were taken at 0700, 0800 and 0900 h, and at 1700, 1800 and 1900 h to measure plasma concentrations of prolactin, LH and progesterone. Administration of RU486 from day 1 of pseudopregnancy onwards had no effect on the increasing concentrations of serum progesterone during the first half of pseudopregnancy. Thereafter progesterone concentrations of serum progesterone during the first half of pseudopregnancy. Thereafter progesterone concentrations increased further in RU486-treated rats whereas they decreased in oil-treated pseudopregnant rats. Administration of RU486 from day 8 of pseudopregnancy onwards resulted in a decline in progesterone concentrations in serum on day 10 followed by ovulation on day 11. Plasma LH concentrations in rats treated with RU486 from day 1 of pseudopregnancy were higher than those in oil-treated rats on days 8, 9, 10 and 11.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Effect of hypothyroidism on the pituitary-gonadal axis in the adult female rat.

The pituitary-ovarian axis was studied after withdrawal of thyroid hormone in 131I-radiothyroidectomized adult female rats. Oestrous cycles became prolonged and irregular within 2 weeks after the supply of thyroid hormone was stopped. If an LH surge occurred in hypothyroid rats on the day of vaginal pro-oestrus it was significantly greater in rats which had been made hypothyroid for 4-5 weeks than in controls; in hypothyroid rats with an LH surge on pro-oestrus, plasma progesterone showed a rise similar to that in controls at pro-oestrus; the ovulation rate was decreased in hypothyroid rats. About half of the rats from which blood was sampled daily in the afternoon between 7 and 18 days after tri-iodothyronine (T3) withdrawal had 1 day of pro-oestrus; on this day the LH surge was higher than in controls. On days 2 and 1 before and days 1 and 2 after this pro-oestrus, plasma progesterone was similar to that of controls on days 2 and 1 before and days 1 and 2 after pro-oestrus respectively. However, progesterone was higher in the period before and after these days. The other hypothyroid rats showed no pro-oestrus and no LH surge during this period, while their plasma progesterone levels were high on all days. On the morning of day 10 after T3 withdrawal and 5 days after the preceding pro-oestrus, most hypothyroid rats had high progesterone and low oestradiol plasma levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Advancement of meiotic resumption in graafian follicles by LH in relation to preovulatory ageing of rat oocytes.

After ovulation, the fertile life of oocytes is short. In the present study, the fertile life of oocytes was studied in relation to the resumption of meiosis. Early on the day of pro-oestrus, meiotic resumption was advanced in rats by a brief infusion of LH; ovulation was induced 8 h later by Ovalyse, a GnRH analogue; rats were mated 13 h after receiving Ovalyse, that is at about the time of ovulation. Rats in which meiosis was not advanced were injected with Ovalyse and mated at various intervals after ovulation. Rats were killed 13 h after mating or on day 20 of pregnancy. In rats in which meiosis was not advanced that were mated around ovulation, fetal survival was about 90%. In rats with meiosis advanced by 8 h and mated around ovulation, only 44% of the ovulated oocytes with advanced meiosis developed into healthy fetuses; mortality before and after implantation was 37 and 19%, respectively. Rats in which meiosis was not advanced that were mated 8-9 h after ovulation had similar fetal survival and similar mortality before and after implantation. Thus ageing of the oocyte may occur either before, or after, ovulation. Preovulatory ageing is related to the resumption of meiosis.

Animals↗

PubMed1993

Advancement of meiotic resumption in graafian follicles reduces fertility in the rat.

Fertile life of oocytes is usually considered to be related to ovulation time. In the present study, fertile life of rat oocytes was studied in relation to resumption of meiosis. In pro-oestrus, meiotic resumption without concomitant ovulation was induced in most graafian follicles by injection of a small amount of LH or FSH followed by Nembutal. These follicles either ovulated or developed into luteinized unruptured follicles if Ovalyse (a GnRH analogue) was given 8 h after LH or FSH. In subsequent experiments, rats were injected with FSH or saline, and Nembutal; 4 or 8 h later, Ovalyse was given to induce ovulation; the rats were mated 14 h after Ovalyse. At day 20 of pregnancy, fetal survival was 30% in rats with meiosis advanced by 8 h, against 91% and 70% in rats advanced by 0 or 4 h, respectively. Mortality occurred mainly during pre-implantation and early post-implantation. Advanced resumption of meiosis may cause pre-ovulatory ageing of oocytes; consequently, viability of these oocytes after ovulation is reduced.

Animals↗

PubMed1992

The effect of decrease in body temperature with Nembutal on meiosis and ovulation after induction by gonadotrophin-releasing hormone and luteinizing hormone in adult rats.

Sodium pentobarbital (Nembutal) is often used to block the pro-oestrous luteinizing hormone (LH) surge in rats. Nembutal is also known to lower body temperature. This study was designed to investigate whether Nembutal affected the time course of meiosis and timing of ovulation induced by exogenous hormones, and whether the possible effects of Nembutal on these processes were related to temperature. Gonadotrophin-releasing hormone (GnRH), the GnRH-analogue Ovalyse, or rat luteinizing hormone (LH) were administered to trigger resumption of meiosis and ovulation; Nembutal (35 mg kg-1 body weight) or saline was given 10 or 60 min later. Plasma profiles of LH were measured and Graafian follicles were studied histologically for meiotic progress and ovulation. Nembutal suppressed the spontaneous surge of LH at pro-oestrus and caused a long-lasting decrease in body temperature. If 1000 ng GnRH was given 2 h before the pro-oestrous LH surge, most of the oocytes had extruded a polar body 10 h later and most follicles had ovulated 14 h later. Nembutal given 1 h after GnRH delayed extrusion of the polar body and ovulation by about 2 h. Nembutal caused a similar delay in ovulation when it was administered after 100 ng of Ovalyse, and it also delayed meiosis when given after 1000 ng of LH. This effect of Nembutal was prevented if body temperature was maintained at 37 degrees C. The delaying effect of Nembutal on meiosis and ovulation induced by exogenous GnRH or LH is related to a long-lasting decrease in body temperature.

Animals↗

PubMed1991

Quantification and classification of pregnancy wastage in 5-day cyclic young through middle-aged rats.

Fecundity was quantified in 4 to 11-month old rats with regular 5-day cycles. On the day following mating, less than 5% luteinized unruptured follicles occurred in either 4-month old or 11-month old rats; ovulation rate and also fertilization rate were similar in these young and middle-aged rats. At day 19 of pregnancy embryonic and fetal mortalities were quantified. Pregnancy wastage increased gradually with age; it was already significant in 7-month old rats. In rats of 9 months old it was about 30% and in 11-month old rats it was greater than 65%. Pregnancy wastage was mainly due to preimplantation and early-postimplantation mortality. Pregnancy wastage did not decrease when the pre-ovulatory surge of luteinizing hormone (LH) was reinforced and timed, by injection of the LH-releasing hormone analogue Ovalyse at noon on the day of prooestrus. The results corroborate the idea that pregnancy wastage in middle-aged rats with regular cycles is caused by an age-related reduction of the viability of ovulating eggs.

Aging↗

PubMed1987

The effect of a single dose of human chorionic gonadotropin at proestrus on embryonic mortality, fetal growth and gestation length in the rat.

The noxious effect of a single dose of 20 IU human chorionic gonadotropin (hCG) given at proestrus on embryonic and fetal survival as well as on fetal weight was studied. Fetal survival varied between 43.6 and 67.6%; the mortality rate was highest before implantation. The surviving fetuses of rats treated with hCG between days 17 and 20 of pregnancy weighed significantly less than controls. Embryonic mortality and fetal growth retardation could be prevented by giving anti-hCG monoclonals 28 or 45 h after hCG administration, but not when anti-hCG was given 69 or 93 h after hCG. 5 IU hCG did not induce embryonic or fetal mortality. On the other hand, 80 IU hCG increased the mortality to 100%; this was entirely due to preimplantation loss. It is speculated that due to a long metabolic half-life of hCG, the steroid metabolism is disturbed, causing implantation failure and/or delay of implantation. By day 21 of pregnancy, however, the fetuses of the hCG-treated rats had made up greatly for the growth retardation; they were born after a similar gestation length and with a similar birth weight as the pups of control rats.

Animals↗

PubMed1986

Administration of human chorionic gonadotropin but not of luteinizing hormone-releasing hormone at pro-oestrus or late di-oestrus has a deleterious effect on pregnancy in the rat.

Embryonic and fetal mortality is studied, which is induced by human chorionic gonadotropin (hCG) and luteinizing hormone-releasing hormone (LHRH) given prior to ovulation. 5-day cyclic rats were injected with 20 IU hCG or with 1 microgram LHRH on day 3 of di-oestrus or on the day of pro-oestrus, and mated 4 h later. Autopsy was performed on day 3 or between days 13 and 18 of pregnancy. Advancement of ovulation by LHRH did not induce embryonic or fetal mortality. Administration of hCG at pro-oestrus or day 3 of di-oestrus induced a considerable mortality, which for the greater part occurred after day 3 of pregnancy but before implantation. This embryonic mortality could be prevented by anti-hCG serum given 21 h after hCG. It is speculated that embryonic mortality induced by hCG is caused by a relatively long-lasting disturbance of steroid metabolism, due to a long metabolic half-life of hCG. The disturbance of steroid metabolism as a possible cause of implantation failure is discussed.

Animals↗

PubMed1982

No evidence for a peripheral effect of L-DOPA on plasma prolactin in the rat.

Male and female rats with two permanently indwelling intravenous catheters were infused for 2 hours with ovine prolactin. During equilibrium conditions the effects of intravenously injected L-DOPA and benzerazide (a blocker of dopa-decarboxylase) on steady state levels of ovine prolactin were measured. A dose of 4.5 mg L-DOPA per 100 gr body weight (b.w.) caused a transient increase of plasma ovine prolactin. A dose of 0.3 mg L-DOPA/100 gr b.w. had no effect, neither in males nor in females, while benzerazide (20 mg/100 gr b.w.) had only a slight effect. The experiments suggest that L-DOPA does not affect the peripheral uptake of prolactin from the plasma.

Animals↗

PubMed1979

The suckling-induced rise of plasma prolactin in lactating rats: its dependence on stage of lactation and litter size.

The response of plasma prolactin in vigorous suckling was measured in lactating rats which had been isolated for 10-12 h from their offspring. Plasma prolactin was investigated during suckling at various stages of lactation. The results demonstrate that prolactin responds maximally to suckling already in the first days of lactation. In the second half of the lactation period, the prolactin rise in the plasma induced by suckling decreases gradually; this is not due to a reduced suck-intensity of older pups. A relationship is found between the height of the suckling-induced prolactin rise and litter size. The data suggest that during suckling in the first weeks of lactation the pituitary secretes large amounts of prolactin at a constant rate. It is speculated that in the first minutes of suckling, receptors may clear considerable amounts of released prolactin from the circulation.

Age Factors↗

PubMed1978

Circadian variations in the plasma concentration of prolactin in the adult male rat.

The occurrence of circadian variations in the concentration of prolactin in the plasma of 6- to 9-month-old male rats has been assessed in animals exposed to light for 14 h/day (lights on 06.00--20.00 h). Blood samples were obtained after decapitation, or from individual rats at regular intervals via a permanent cannula. Care was taken to limit stress during sampling. The concentration of prolactin in the plasma was significantly lower between 07.00 and 15.00 h than at other times. Between 15.00 and 20.00 h (during the light period), the concentration of prolactin was significantly higher in comparison with the preceding period, or with the remainder of the 24 h period. During the night, the concentration fluctuated, probably because of episodic releases of the hormone. The possible physiological significance of a circadian rhythm in the plasma concentration of prolactin and the implications for endocrine experimentation are discussed briefly.

Animals↗

PubMedDate not supplied

Intraperitoneal infusion of EDTA in the rat blocks completely the prolactin rise in the plasma during suckling.

Lactating rats supplied with chronically indwelling intravenous (i.v.) and intraperitoneal (i.p.) catheters were allowed to suckle after a night of isolation from their offspring. The effect of infusions of saline and EDTA, given i.v. or i.p. on the suckling-induced rise of plasma prolactin was evaluated by radioimmunoassay. i.v. saline and EDTA did not affect the normal prolactin rise induced by suckling. However, i.p. EDTA completely blocked this rise, while the weight gain of the pups during the suckling period was only slightly depressed. i.p. EDTA had no suppressive effect on the perphenazine-induced rise of plasma prolactin and caused only a moderate inhibition of the prolactin rise in the plasma evoked by thyrotropin-releasing hormone and by brief exposure to ether. The experiments indicate, that because i.p. EDTA probably stimulates dopamine only slightly, it must inhibit prolactin secretion via another mechanism. This study, therefore, strongly supports the idea that more than one hypothalamic factors affect prolactin release during suckling.

Animals↗