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Biomedical subjects

J Schoemaker

Publications and source records attributed to J Schoemaker.

At least 145 records · Page 8Linked to original sources
PubMed1987

Phenobarbital enhances pituitary LH release induced by LRH pulses in the ovariectomized rat.

In the ovariectomized (OVX) rat, the plasma LH response was measured to a pulse of LRH (1.25 or 5 ng/100 g body weight, ia) given before and 1 h after ip administration of phenobarbital (80 mg/kg body weight). The LH response to the LRH pulses was increased 1 h after phenobarbital. In a second experiment, the pituitary LH content of OVX rats was measured 1 h after administration of phenobarbital or saline. No difference in pituitary LH content was found. It is concluded that in the OVX rat, phenobarbital increases the response to a pulse of LRH, presumably by suppressing endogenous pulsatile LRH. This, together with results of earlier experiments, further supports the hypothesis that under conditions where endogenous pulsatile LRH is present, there is always a certain degree of pituitary desensitization or refractoriness and that the removal of this endogenous LRH leads to recovery of pituitary sensitivity to LRH.

Animals↗
PubMed1987

Patterns of LH and FSH in men during high-frequency blood sampling.

The aim of the study was to test the hypothesis that in serial determinations of concentrations of LH and FSH involving blood samples taken every minute, the observed pulses of LH and FSH which last less than 3-4 min might not be a physiological phenomenon but part of the 'noise' of the radioimmunoassay or blood-sampling technique. Blood was sampled every minute for a period of 90 min in six men. During the first 45 min, blood was sampled by means of vacuum tubes only. During the second 45 min, sampling took place with a syringe via a rubber stopper, either using a tourniquet (n = 3) or flushing the cannula with heparinized saline. Three criteria were used to identify variations in the patterns of LH and FSH as true hormonal changes. First, a threshold was used which had to be exceeded by the difference between nadir and maximum values before a pulse could be identified. An average of approximately six pulses per 90 min was found in both the LH and FSH series. The majority of these pulses lasted less than 3-4 min. In two subjects, larger LH pulses of longer duration were measured. Secondly, differences between duplicate measurements of nadir and/or maximum values of more than one-third of the amplitude of a pulse were considered unacceptable. This involved about 75% of the pulses. Thirdly, the reproducibility of the hormone variations was estimated. In one subject, concentrations of LH were measured four times in four separate assays.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Ovulation induction with pulsatile luteinizing releasing hormone in women with clomiphene citrate-resistant polycystic ovary-like disease: clinical results.

Eighty-four treatment units were given to 11 women with clomiphene citrate-resistant polycystic ovarian disease (PCOD). PCOD was defined as oligomenorrhea elevated luteinizing hormone (LH), normal follicle-stimulating hormone (FSH), and preference-elevated androgens. Luteinizing-releasing hormone (LRH) was administered intravenously via a portable infusion pump. Doses varied between 5 and 40 micrograms/pulse given at 60-, 90-, or 120-minute intervals. In 11 women, 85 treatment units (TUs) were completed, of which 74 were ovulatory, showing no specific advantage of any particular pulse dose or pulse interval. Five pregnancies occurred in three women. Two women did not ovulate during 52 and 284 consecutive days of therapy, respectively. Oligomenorrheic patients with PCOD can be made more regular by means of LRH, not necessarily leading to a regular menstrual cycle. In general, LRH is sufficient for luteal support. No signs of hyperstimulation were observed, although two patients incidently developed unilocular cysts with a maximum diameter of 8 cm. Ovulation induction with LRH in PCOD is possible, although the disease itself does not change during therapy. This may be further evidence that altered hypothalamic LRH secretion is more the result, rather than the cause, of the phenomenon of PCOD.

17-Ketosteroids↗
PubMed1986

Short-term pituitary desensitization to LH-RH after pulsatile LH-RH in the ovariectomized rat: an in vivo experiment.

The development of acute insensitivity of pituitary LH secretion to LH-RH after a short exposure to LH-RH is described. In the first experiment, ovariectomized (OVX), phenobarbital-pretreated rats were given pulses of LH-RH (1.25 or 6.25 ng/100 g body weight (b.w.), intravenously). In rats given 1.25 ng at time 0, 6.25 ng at 60 min, 1.25 ng at 80 min and 1.25 ng at 120 min, there was a substantial increase in plasma LH after the first two injections, no increase after the third injection and a relatively small increase after the fourth one. In other rats treated identically but not given a 1.25-ng dose at 80 min, the plasma LH rise in response to the 1.25-ng dose at 120 min was comparable to that seen after the 1.25-ng dose given at time 0. If the 1.25-ng LH-RH pulses given at times 0 and 80 min were replaced by a rat pituitary extract, the plasma LH rise in response to the 1.25-ng dose at 120 min was comparable to that seen after administration of pituitary extract. In the second experiment, OVX phenobarbital-pretreated rats were given 1.25 ng LH-RH/100 g b.w. at t = 0. They were then divided into three groups, each receiving 1.25, 3.75 or 6.25 ng LH-RH/100 g b.w. at t = 60 min. Each of these three groups was again divided into three groups which received 1.25 ng LH-RH/100 g b.w. at 80, 100 or 120 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Prolonged pulsatile administration of luteinizing hormone-releasing hormone in prepubertal children: diagnostic and physiologic aspects.

In order to test gonadotropic function 30 prepubertal and 2 early pubertal girls and boys were treated with LH-releasing hormone (LRH) in a pulsatile fashion for 7 days. LRH was administered iv either in a dose of 10 micrograms every 90 min or in a dose of 20 micrograms/1.73 m2 every 96 min. On days 1 and 7, just before as well as at the end of LRH treatment, a LRH test (100 micrograms/m2 iv) was performed. In 27 patients a LRH test was repeated 4 (day 11) or 7 days (day 14) after LRH withdrawal as well. Plasma LH, FSH, and estradiol or testosterone levels were estimated during the LRH tests on days 1, 7, and 11/14. The patients were divided into 4 groups: group 1 consisted of 2 girls and 1 boy with gonadal failure, group 2 of 1 girl and 2 boys with intact pituitary and gonadal function, group 3 of 11 girls and 13 boys with various central endocrine disorders, and group 4 of 1 girl and 1 boy with pubertal arrest of unknown origin. In group 1 LRH treatment elicited an increase of both gonadotropins into the castrate range, whereas gonadal steroids did not increase. In group 2 baseline LH as well as the response to LRH increased on day 7. In the boys FSH changed similarly. In the girl baseline FSH increased, but the high FSH response of day 1 decreased. Estradiol and testosterone levels were elevated on day 7. These changes during LRH treatment are similar to those during normal pubertal development. When the LRH test was repeated on day 11/14 basal levels had returned into the prepubertal range and a high response of LH especially was found in all 3 subjects. Patients of group 3 were separated into two subgroups: group 3a, those with, and group 3b, those without an increase of gonadal steroids on day 7 of LRH treatment. Since an increment must be the result of increased gonadotropin stimulation, this probably indicates intact gonadotropic function. Group 3a had a pattern of gonadotropin secretion similar to group 2. In group 3b basal and peak LH levels were lower on day 7 compared to group 3a, whereas FSH levels did not differ. Four or 7 days after LRH discontinuation (day 11/14) basal gonadotropin levels were in the original low range. In the LRH test mean LH peak level of group 3a was 43.7 U/liter, of group 3b 13.1 U/liter (P less than 0.01).(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1985

Pulsatile luteinizing hormone patterns in the follicular phase of the menstrual cycle, polycystic ovarian disease (PCOD) and non-PCOD secondary amenorrhea.

To characterize the oscillations of plasma LH in normally cycling and amenorrheic women, three groups of women were studied: I, normal women during the follicular phase of the cycle (n = 9); II, women with polycystic ovarian disease (PCOD; n = 11); and III, women with non-PCOD secondary amenorrhea (n = 12). Blood samples were obtained at 10-min intervals for 6 h on 2 separate days. A pulse was defined as an increase in LH at least 20% over the preceding lowest value (nadir). Since LHRH release immediately follows the nadir of the LH levels, the nadir interval (NI) was used for analysis. For analysis, the results from 1 day were selected at random from each subject, and from each day, the same number of NIs also were randomly selected. When two NIs from each patient were selected, the median NI was 75 min in group I, 45 min in group II, and 45 min in group III. When three or four NIs were chosen, the median NI was 60 min in group I, 50 min in group II, and 40 min in group III. The differences between the groups were statistically significant. When three NIs were selected, the mean of the corresponding LH amplitudes was 2.8 U/liter in group I, 6.0 U/liter in group II, and 1.5 U/liter in group III. The differences between these groups were statistically significant. Thus, the NI in PCOD patients was shorter than that during the follicular phase of the cycle, but this short NI is not unique for PCOD, since the NI in non-PCOD secondary amenorrhea patients was even smaller. The LH amplitude was higher in PCOD and lower in non-PCOD secondary amenorrhea compared to that during the follicular phase of the cycle. The decrease in NI in PCOD and/or non-PCOD secondary amenorrhea vs. the NI of the follicular phase could be explained by either a higher frequency of LHRH pulses from the hypothalamus or an increased sensitivity of the pituitary leading to a greater response of the pituitary to LHRH pulses.

Adolescent↗
PubMed1984

Prolonged pulsatile LRH treatment in different frequency schedules in a hypogonadotropic male.

A 22 years old male patient with a pubertal arrest of unknown origin at P4, G3 received LRH in three different schedules, each lasting for four weeks. 8 times per day 20 micrograms LRH iv, 16 times per day 20 micrograms LRH iv, 32 times per day 20 micrograms LRH iv. During the first period the low FSH levels increased into the normal adult range, while LH remained at the low level, a change also observed in early puberty. Testosterone increased to low normal adult values. In the second period LH as well as testosterone increased to normal adult values and in the third period LH, FSH as well as testosterone increased into the high normal range. There was no evidence of desensitization of the gonadotrophic cells during the third period. From these data we suggest that: 1. LRH treatment in a frequency higher than physiologic, as observed in adult men, does not result necessarily in desensitization of the gonadotrophic cells and 2. the change in gonadotropin secretion in early puberty may be the result of an increased LRH stimulation in a frequency lower than observed in adults.

Adult↗
PubMed1983

Oestrogens induce an LH surge in a prepubertal patient with 45,X gonadal dysgenesis under prolonged pulsatile LRH administration.

A nine year old prepubertal patient with 45,X gonadal dysgenesis received pulsatile LRH administration for 3 weeks, every 90 min 10 micrograms iv. In the first week LH and FSH levels increased from prepubertal levels into the castrate range. Under 2.5 micrograms ethinyloestradiol (EE) LH levelled off for 3 days, followed by an LH surge. FSH showed an ethinyloestradiol dose-dependent decrease. These data suggest that: 1) pulsatile LRH administration may help to distinguish prepubertally those Turner patients with potential ovarian function from those without; 2) oestrogens exert both a negative and positive feedback action at the pituitary level in the LRH treated human; 3) the pituitary does not need 'pubertal maturation' for developing positive feedback to oestrogens. This supports the notion that pubertal maturation is confined to suprapituitary changes.

Child↗
PubMed1983

Induction of puberty by prolonged pulsatile LRH administration.

Pubertal maturation was induced in a 17.7 year old hypogonadotrophic boy by pulsatile LRH treatment. LRH was administered in three periods. During period one 20 micrograms LRH pulses were given iv 16 times per day for 10 weeks; during period two 2 micrograms LRH pulses iv 16 times per day for 12 weeks. During period three 2 micrograms LRH pulses 16 times per day were given sc for 13 weeks. Treatment was interrupted for 6 weeks between period one and two. Rapid initiation of pubertal maturation was evidenced by an increase of penile length and testicular volume as well as by growth of pubic hair. After 21 weeks of treatment spermatozoa were observed in the ejaculate. Gonadotrophin levels increased from prepubertal values into the supranormal range in the beginning of period one, spontaneously declining to normal adult levels. A rapid increment of testicular volume during period one was also evidence for overstimulation. During period two gonadotrophin levels were in the normal range. Testosterone levels were normal during period one and two albeit higher during period one. We conclude that 1) pulsatile LRH treatment with 2 micrograms per pulse iv 16 times per day is an adequate and feasible way to induce puberty in hypogonadotrophic males with an intact pituitary. 2) Under pulsatile LRH treatment spermatogenesis takes place more rapidly than during normal puberty. 3) Testicular hormones exert a negative feedback action at the pituitary in the LRH treated hypogonadotrophic male. 4) The supranormal levels of LH and FSH during the first weeks of treatment may be caused by a delayed reaction of the testicles to gonadotrophin stimulation rather than to an overdose of LRH. 5) No evidence was found of a direct inhibitory action of LRH on testicular function.

Adolescent↗
PubMed1983

Induction of ovulation by prolonged pulsatile administration of luteinizing hormone releasing hormone (LRH) in patients with clomiphene resistant polycystic ovary-like disease.

Induction of ovulation with pulsatile administration of LRH by automatic portable infusion pump for 74 and 147 consecutive days in 2 patients with clomiphene resistant PCO-like disease is described. The patients exhibited 6 ovulatory cycles. One patient conceived during the fourth cycle. During the treatment a unilocular cyst, probably a lutein cyst, developed in one patient, but subsequently disappeared spontaneously under uninterrupted therapy. No chemical hyperstimulation was observed. Follicular phases lasted for 32 and 13 days in patient I and for 19, 25, 14 and 22 days in patient II. Luteal phases lasted for 16 and 15 days in patient I and for 17, 18 and 15 days, respectively in patient II. Total urinary oestrogen and pregnanediol excretion did not differ from that seen in normal cycles. LH baseline and peak values and LH responses declined to normal levels accompanied by a normalization of the LH/FSH ratio during pulsatile LRH treatment in both patients. The first pre-ovulatory episode occurred already after partial normalization of the LH/FSH ratio. The endocrinology of the second LRH induced cycles of patients I and II was not different from cycles similarly induced in hypogonadotrophic patients. We conclude that ovulation induction with pulsatile LRH administration in patients with clomiphene resistant PCO-like disease is possible. Our findings give hope that this mode of treatment may not only be effective, but may prove to be safer than ovulation induction with menopausal gonadotrophins in patients with clomiphene resistant PCO-like disease.

Adult↗
PubMed1982

Immunoreactive beta-endorphin in the hypothalamus of female rats: changes in content and release during prepubertal development.

Female Wistar rats of different ages (1-45 days) were used. Extracts were made of the mediobasal hypothalamus (MBH) and beta-endorphin immunoreactivity (beta-ENDi) was quantitated by radioimmunoassay. Low but significant amounts of beta-ENDi (6.5 ng/MBH) were present on the first postnatal day. Hypothalamic beta-ENDi content did not change during the first week but decreased during the second week to a minimum (4.5 ng/MBH) on day 14. Thereafter, beta-ENDi increased rapidly to 13 ng/MBH on day 28 and remained at this level. Gel filtration showed that beta-ENDi substances with chromatographic characteristics identical to those of beta-END and beta-LPH were present in MBHs of 14-, 20- and 45-day-old rats. A beta-ENDi substance, possibly representing beta-END1-27, was nearly absent on day 14, but represented a major component of the MBH of the 45-day-old rat. In vitro incubation of MBH resulted in spontaneous release of beta-ENDi. Depolarization of neuronal membranes by incubation in medium containing 45 mMK+ stimulated beta-ENDi release. Both the spontaneous and K+-stimulated release of beta-ENDi were low on day 10 but reached postpubertal levels on day 20. These observations lead us to propose that the beta-ENDi-containing neurons in the hypothalamus of developing female rats rapidly mature between 14 and 20 days after birth. This may be causally related to the rapid decrease in circulating FSH levels that occurs during this period.

Aging↗
PubMed1982

Ultrasonographic measurement of the yolk sac.

Ultrasonographic measurements of the yolk sac were made during first trimester in 100 pregnancies. The results were related to the crown-rump length of the embryos and showed an increase in size from 7 to 11 weeks menstrual age. A possible relation between anomalies in yolk sac development and embryonic development was studied in six patients by means of serial weekly ultrasonographic examinations. In one case with absence of the yolk sac embryonic death occurred at 10 weeks menstrual age; the embryo had spina bifida.

Anthropometry↗
PubMed1982

In vitro release of LHRH from the hypothalamus of female rats during prepubertal development.

In this study changes in serum FSH concentration, hypothalamic LHRH content and in vitro release of LHRH from hypothalami of female Wistar rats during prepubertal development are described. The concentration of FSH in serum was determined by radioimmunoassay. Extremely high levels (1.800 ng/ml) were found between 12 and 16 days of age. Thereafter, FSH levels rapidly fell to low levels (135 ng/ml) on day 32. LHRH was measured by radioimmunoassay in extracts of mediobasal hypothalami (MBH) and showed a gradual increase during the first 10 days of life. Between 10 and 16 days of age, hypothalamic LHRH content did not change. After day 16, LHRH content sharply increased to a maximum found on day 32. The release of LHRH from MBH of developing rats was studied during in vitro incubation in Krebs-Ringer bicarbonate buffer. LHRH in the medium was measured by radioimmunoassay. The spontaneous release rate of LHRH was maximal from MBH of 12-day-old rats and minimal from those of 32 days. Depolarization of neural membranes, by medium containing 45 mM K+ induced a stimulation of LHRH release. This K+ -induced release of LHRH was also most prominent on day 12. These observations are consistent with the hypothesis that the high circulating FSH levels found in female rats between 12 and 16 days of age are at least in part caused by a high secretion rate of LHRH during this period.

Animals↗
PubMed1981

X-autosome translocation with a breakpoint in Xq22 in a fertile woman and her 47,XXX infertile daughter.

An unusual case is presented of a fertile woman heterozygous for a balanced X-autosome translocation t(X;12)(q22;p12) with a break-point (Xq22) in the critical region of the X chromosome. The karyotypes of her daughter, who is infertile, and one of her two sons are 47,XXX,t(X;12)(q22;p12) and 46,XY,t(X;12)(q22;p12) respectively. The literature on balanced X-autosome translocations in males and females involving both arms of the X chromosome is reviewed. All 23 of the 36 cases of females with balanced Xq-autosome translocation, that exhibited gonadal failure have a break-point between bands Xq13 and Xq26.U

Adult↗
PubMed1981

Pregnancy after prolonged pulsatile administration of luteinizing hormone-releasing hormone in a patient with clomiphene-resistant secondary amenorrhea.

Induction of ovulation with LRH, self-administered by the patient (20 microgram every 2 h, iv) from 0700-2300 h continuously for 90 days, is described. Three ovulatory cycles resulted, and the patient conceived during the third cycle. The morning serum LH and FSH concentrations showed a pattern similar to that seen in normal cycles. Total urinary estrogen and pregnanediol excretion did not differ from those in normal cycles. This observation shows that the described mode of treatment is feasible and can result in normal intrauterine pregnancy.

Amenorrhea↗