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Biomedical subjects

A N Andersen

Publications and source records attributed to A N Andersen.

15 recordsLinked to original sources
PubMed1991

Intrauterine fertilization capsules--a clinical trial.

Treatment of 26 women with tubal infertility was attempted using intrauterine capsules loaded with oocytes and spermatozoa. The stimulation protocol was as used for in vitro fertilization and embryo transfer and consisted of short-term use of Buserelin, human menopausal gonadotropin, and human chorionic gonadotropin. Oocytes were collected by ultrasonically guided transvaginal aspiration, and spermatozoa were prepared by swim-up technique. The gametes were placed in agar capsules 4 hr after oocyte collection, and the capsules were introduced to the uterine fundus using an insertion tube and piston from an intrauterine device. Six complete capsules and parts of two other capsules were expelled. None of the women became pregnant, compared with a pregnancy rate of 21% per aspiration following in vitro fertilization and embryo transfer during the same period.

Buserelin↗
PubMed1991

Pulsatile gonadotropin secretion and basal prolactin levels during dopamine D-1 receptor stimulation in normal women.

The effect of the specific dopamine D-1 receptor agonist Fenoldopam on pulsatile gonadotropin secretion and prolactin (PRL) secretion was investigated in normal women. The gonadotropin response to subsequent gonadotropin-releasing-hormone (GnRH) administration was also studied. Eight women received 8-hour infusions of either Fenoldopam (0.5 microgram/kg per minute) (Smith Kline and French, Harrow, United Kingdom) or placebo. After 7 hours of infusion, GnRH was given intravenously. The luteinizing hormone (LH) response to GnRH was significantly higher during Fenoldopam compared with placebo (LH; 13.1 +/- 9.0 versus 9.4 +/- 4.3 IU/L). Basal LH levels, pulse amplitude, and pulse frequency during Fenoldopam infusion were not different from placebo. Prolactin levels increased significantly during Fenoldopam (24 +/- 2 micrograms/L) compared with placebo (16 +/- 2). The results suggest that D-1 receptor stimulation does not affect pulsatile gonadotropin secretion but increases the pituitary responsiveness to GnRH. Additionally, dopamine and Fenoldopam have opposite effects on PRL secretion, the latter increasing PRL levels.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1990

[Goserelin].

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Buserelin↗
PubMed1990

Effect of dopamine and a dopamine D-1 receptor agonist on pulsatile thyrotrophin secretion in normal women.

The inhibitory effect of a pharmacological dose of dopamine and the specific dopamine D-1 receptor agonist fenoldopam on basal and pulsatile TSH secretion was investigated in normal women. The TSH response to fenoldopam and subsequent releasing hormone administration was also studied. Six women received placebo or dopamine infusion (4.0 micrograms/kg min) for 17 h. After 9 h, blood samples were collected every 10 min between 0800 and 1600 h for measurement of TSH. Eight women received 8-h (0900-1700 h) infusions of either fenoldopam (0.5 micrograms/kg min) or placebo. After 7 h of infusion 10 micrograms TRH, 5 micrograms GnRH and 25 micrograms CRF was given i.v. Blood samples were collected every 10 min. Dopamine infusion as well as fenoldopam infusion significantly reduced both mean basal TSH secretion and TSH pulse frequency compared with corresponding control infusions (P less than 0.05). However, while the effect on TSH pulsatility was comparable (P greater than 0.05), the percentage decrease in basal TSH levels after 16 h of dopamine infusion was 51 +/- 16% (mean +/- SD) and after 7 h of fenoldopam infusion 19 +/- 12% (P less than 0.05). Neither of the drugs affected TSH pulse amplitude and fenoldopam did not influence TRH-stimulated TSH release (P greater than 0.05). The results suggest that dopamine D-1 receptors are involved in modulation of TSH pulsatility probably at the hypothalamic level. It is argued that dopaminergic inhibition of basal TSH secretion and TSH pulsatility is predominantly regulated through dopamine D-2 receptors at the pituitary level, and through D-1 receptors at the hypothalamic level, respectively.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1990

Effect of dopamine, dopamine D-1 and D-2 receptor modulation on ACTH and cortisol levels in normal men and women.

The regulation of the hypothalamic-pituitary-adrenal axis by dopamine is not fully understood. Therefore, we have studied the effect of dopamine, metoclopramide, a D-2 receptor antagonist, and fenoldopam, a specific D-1 receptor agonist, on ACTH and cortisol levels in normal subjects. Normal women received 5-h infusions of either glucose (N = 6) or dopamine at rates of 0.04 (N = 6), 0.4 (N = 6) and 4.0 micrograms.kg-1.min-1 (N = 8). After 3 h, 10 mg metoclopramide was given iv. No intergroup differences regarding ACTH and cortisol levels were observed (p greater than 0.05). In a second study six women received dopamine (4.0 micrograms.kg-1.min-1) or glucose for 18 h. During the infusions cortisol and ACTH levels were similar on the two study days. Administration of metoclopramide (10 mg) after 17 h induced a significant increase in cortisol levels during dopamine infusion (p less than 0.05), whereas no effect was observed during placebo infusion. ACTH levels were unaffected by metoclopramide. In a third study, 9 normal women and 9 normal men received fenoldopam (0.5 micrograms.kg-1.min-) or placebo infusions for 3 h. In males, median ACTH and cortisol levels were significantly lower (p less than 0.05) during fenoldopam compared with placebo infusion. In contrast, fenoldopam did not affect ACTH and cortisol levels in normal women. The results suggest that the effect of dopamine D-1 receptor stimulation on ACTH and cortisol secretion is mainly at the hypothalamic level and that this effect is sex-dependent.(ABSTRACT TRUNCATED AT 250 WORDS)

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1979

[Mastalgia].

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Breast Diseases↗
PubMed1979

Treatment of hyperprolactinemic luteal insufficiency with bromocriptine.

Twelve patients with infertility and insufficent luteal function were studied during a control cycle, and during a cycle when 2.5 mg of bromocriptine was given twice daily. Serum levels of prolactin, progesterone, estradiol-17-beta, FSH and LH were determined during both cycles. Endometrial biopsies were taken from most patients during the late luteal phase. Two patients had persistent hyperprolactinemia, approximately 35-45 ng/ml, and both had repeated insufficient luteal function, which completely reverted to normal during treatment. Five of the 10 normoprolactinemic patients achieved a normal luteal function during bromocriptine therapy. No pregnancies were achieved during the study but one patient later conceived during bromocriptine therapy.

Adult↗
PubMed1979

Plasma enteroglucagon after jejunoileal bypass with 3:1 or 1:3 jejunoileal ratio.

Enteroglucagon concentration in peripheral blood was determined before and after a test meal in 24 morbidly obese patients. Eighteen had jejunoileal bypass, 6 with a 3:1 and 12 with a 1:3 jejunoileal ratio of the functioning segment, and 6 were unoperated. All three groups exhibited an increment of enteroglucagon concentration after the meal. Both the fasting values and the postprandial integrated increments were higher in operated patients than in unoperated patients and higher after 1:3 bypass than after 3:1 bypass. The findings agree with the hypothesis that enteroglucagon secretion is stimulated by exposure of the lower bowel to upper-bowel content, and that the effect of enteroglucagon is, as seen after bypass operation, stimulation of growth and reduction of motility of the intestine.

Adult↗
PubMed1978

Correlations between prolactin and progesterone, oestradiol-17-beta and oestriol during early human pregnancy.

The correlations between serum prolactin and progesterone, oestradiol-17-beta and oestriol were determined in 125 pregnant females between the sixth and fourteenth week of pregnancy. No significant correlations were found between prolactin and progesterone. Correlations between prolactin and oestradiol-17-beta and oestriol were mostly positive, but only significant during the twelfth week of pregnancy.

Estradiol↗
PubMed1977

Effect of bromocriptine on the premenstrual syndrome. A double-blind clinical trial.

Twenty-one patients suffering from the premenstrual syndrome were each studied during three menstrual cycles. After a control cycle, bromocriptine and placebo were given during the luteal phase of the cycle in a random double-blind cross-over manner, each patient serving as her own control. The dosage of bromocriptine was 2-5 mg twice daily. Serum prolactin levels were found to equal during the follicular and luteal phases, except when reduced by bromocriptine. Serum progesterone and oestradiol-17-beta were within normal ranges, and did not change during treatment. Medication considerably improved all the premenstrual symptoms, but mastodynia was the only one where bromocriptine was significantly better than the placebo.

Adolescent↗