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Biomedical subjects

H Seeger

Publications and source records attributed to H Seeger.

At least 91 records · Page 5Linked to original sources
PubMed1996

Urinary excretion of relaxin after estradiol treatment of postmenopausal women.

The influence of estradiol treatment on the urinary excretion of relaxin, a hormone in earlier years only found during pregnancy and presently associated with functions in the cardiovascular system, was investigated in postmenopausal women. Thirteen postmenopausal women were treated with transdermal estradiol and 12 women with oral estradiol for 4 weeks. A new radioimmunoassay for human-relaxin (rec-hRLX-2) was used. With transdermal, but not with oral administration, a significant increase of urinary relaxin excretion was registered. Further experiments are necessary to elucidate the source of urinary relaxin and its role in the hormone replacement therapy of postmenopausal women.

Administration, Cutaneous↗
PubMed1996

Calciumantagonistic effect of natural and synthetic estrogens--investigations on a nongenomic mechanism of direct vascular action.

Cardiovascular effects of estrogens have been shown to be of great clinical importance treating patients with hormonal replacement therapy or using oral contraceptives. To test one nongenomic mechanism of direct vascular action, the calcium-antagonistic effect of natural and synthetic estrogens was investigated in cell cultures of human vascular muscle cells. 17 beta-estradiol significantly inhibited calcium influx at the concentrations of 10(-6) and 10(-7) M in resting and activated cells. Neither the natural estrogens, estrone, and estriol nor the synthetic estrogens, 17 alpha-estradiol and 17 alpha-ethinylestradiol, significantly changed calcium homeostasis in these cells. The results suggest that the vasodilatory effect of 17 beta-estradiol, seen with hormone substitution in postmenopausal women, could be mediated at least partly via influence on calcium homeostasis.

Analysis of Variance↗
PubMed1995

Improved automated leucocyte counting and differential in newborns achieved by the haematology analyser CELL-DYN 3500.

Automated leucocyte counts in newborns generated by the impedance principle are artificially affected by the high osmotic resistance of some newborn RBC and possibly by the high normoblast numbers present during the neonatal period. Erroneously high WBC counts may result. The haematology analyser CELL-DYN 3500 (Abbott Diagnostika GmbH, Wiesbaden-Delkenheim, Germany) has two different channels for the WBC count, an electrical resistivity (impedance) channel and a laseroptical channel. In combination with facultative extended lysis of resistant RBC before WBC count, this instrument is claimed to be very suitable for newborn blood analysis. We measured the WBC count and differential of 165 blood samples from newborns and cord blood on the CELL-DYN 3500. Reticulocyte count and manual differential including normoblasts were determined. Furthermore, some technical aspects of neonatal blood analysis were evaluated: precision, cell stability, effect of incorrect blood-anticoagulant ratio of small blood collecting tubes. The internal decision making process of the CELL-DYN 3500 selects the result either from the optical channel (identifies and excludes normoblasts) or from the resistivity channel (eliminates resistant RBC). This instrument gives a reliable and accurate WBC count and differential of neonatal samples even in blood samples with normoblasts and lytic resistant RBC. The result given by the CELL-DYN 3500 can be confirmed by a subsequent run in extended lyse mode.

Artifacts↗
PubMed1995

The effect of estradiol on the production of melatonin in postmenopausal women.

The influence of two routes of estradiol administration on pineal melatonin production in postmenopausal women was investigated. Both transdermal and oral estradiol treatment led to an increase as well as decrease of melatonin production in different patients. The reason why individuals respond either in a stimulatory or inhibitory manner is unknown and requires to be evaluated in further more extensive studies.

Administration, Cutaneous↗
PubMed1994

The effect of zearalenone and 17 beta-estradiol on prostacyclin and thromboxane production in cell cultures from human umbilical cord veins.

The effect of zearalenone, a nonsteroidal mycotoxin with estrogenic activity, and of 17 beta-estradiol on prostacyclin and thromboxane production in human endothelial cells was investigated. Zearalenone stimulated prostacyclin production in low concentrations (10(-7) and 10(-8)M) and inhibited it at a higher concentration (10(-5)M). Estradiol alone in the concentration range 10(-5)-10(-8)M had no clear-cut effect on the prostacyclin production. The combination of both substances effected changes in prostacyclin production similar to that from zearalenone alone; with the exception of estradiol at a concentration of 10(-6)M which enhanced the effect of zearalenone. No distinct changes in the thromboxane production from the two substances could be found, either alone or in combination.

6-Ketoprostaglandin F1 alpha↗
PubMed1994

Cardiovascular protection by postmenopausal estrogen replacement therapy: possible mechanisms of the estrogen action.

Estrogen replacement therapy reduces the cardiovascular risk in postmenopausal women, but the mechanism has yet to be evaluated. There is growing evidence that estradiol administration results in direct vasodilatory effects on vessel walls. The biochemical mechanisms have been investigated in human arteries and veins with respect to different mediators and cell systems. Whereas estradiol had no direct effect on the prostaglandin system we found a endothelin-mediated stimulation of prostacyclin production in endothelial cell cultures. In experiments with the NO/cGMP-system estradiol activity could be demonstrated. In addition estradiol provoked an increase in the intracellular Ca2+ concentration. These results indicate that several mechanisms may be involved in the vasodilating effect of estradiol.

Calcium↗
PubMed1994

[Does estradiol modify the NO/cGMP system of blood vessels? Studies of the mechanism of cardiovascular protection by estrogen substitution in the postmenopausal period].

The effect of estradiol on the vasodilating NO/cGMP-system has been investigated in vitro and in vivo. Measurements of cGMP were carried out, cGMP values reflecting NO production. The incubation of human leg vein homogenates (n = 15) for 15 min. with estradiol in the concentrations 10(-6) M, 10(-7) M and 10(-8) M showed at 10(-8) a slight increase of the cGMP-concentrations. Due to high variation compass the difference to the control value was not statistically significant. The clinical part of the study included postmenopausal women, 20 were treated with transdermal estradiol patches (TTS, 0.05 mg/die) and 20 with estradiolvalerate orally (2 mg/die). There were 3 drop outs, 1 in the transdermal estrogen group, 2 in the oral estrogen group. In both groups there were no considerable differences in urinary cGMP concentrations. Thus, these results didn't clearly indicate an involvement of the NO/cGMP-system in the cardioprotective effect of an estrogen substitution therapy in postmenopausal women. Since former investigations are indicative of complex interactions of different vasoactive systems and of the requirement of longer treatment periods for an action of estradiol, an effect on the NO/cGMP-system cannot be ruled out.

Administration, Cutaneous↗
PubMed1993

Natural and synthetic estrogens and prostacyclin production in human endothelial cells from umbilical cord and leg veins.

We have evaluated the effects of 17 beta-estradiol and 17 alpha-ethinylestradiol on prostacyclin production (measured as prostaglandin-6-keto-F1 alpha) in human endothelial cell cultures that had been obtained from umbilical cord and from leg veins. Endothelial cultures were treated with the estrogens at 3 different concentrations (10(-6), 10(-7), 10(-8) M) for up to 72h. 17 beta-estradiol did not affect basal 6-keto-PGF1 alpha production in these cell cultures. With 17 alpha-ethinylestradiol the synthesis of 6-keto-PGF1 alpha was not statistically significant changed. At least in our in vitro system we could not find an effect of natural and synthetic estrogens on 6-keto-PGF1 alpha production. This does, of course not rule out an effect in the more complex in vivo-situation.

6-Ketoprostaglandin F1 alpha↗
PubMed1993

The effect of 17 beta-estradiol and endothelin 1 on prostacyclin and thromboxane production in human endothelial cell cultures.

The effect was investigated of endothelin 1 and 17 beta-estradiol on prostacyclin and thromboxane A2 production (determined as the stable metabolites 6-keto-PGF1 alpha and thromboxane B2, respectively) in endothelial cell cultures obtained from veins of human umbilical cord. There was a statistically significant increase of 6-keto-PGF1 alpha production with endothelin 1 at concentrations of 10(-8) and 10(-9) M [9.5 +/- 1.1% and 7.2 +/- 0.9%, (mean +/- SD, n = 5), respectively] compared to basal production. In contrast, 17 beta-estradiol alone (10(-6) and 10(-8) M) had no effect. In the presence of 17 beta-estradiol (10(-8) M) the stimulating effect of endothelin 1 (10(-8) and 10(-9) M) on 6-keto-PGF1 alpha production was further enhanced to 60.0 +/- 22.5% and 39.5 +/- 22.1%, respectively, compared to basal values. With respect to thromboxane B2, no change in its production was observed by the addition of endothelin 1 and 17 beta-estradiol, alone or in combination in the concentrations mentioned above. These results indicate that 17 beta-estradiol potentiates the effects of endothelin 1 on prostacyclin production in human endothelial cells.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Eicosanoid production in human umbilical cord vessels: effect of 17 beta-estradiol.

This study was designed to investigate the effects of 17 beta-estradiol on prostanoid formation from exogenous arachidonic acid in homogenates of human umbilical cord vessels. The veins produced more prostanoids than the arteries and predominantly 6-keto-PGF1 alpha. 17 beta-estradiol had no effect on the rate of production of prostanoids in either vessels. Thus, at least in our in vitro system, the regulation of the vascular tone by prostanoids seems not to be altered by the addition of 17 beta-estradiol.

Arachidonic Acid↗
PubMed1992

[Production of prostacyclin in human umbilical cord blood vessels. Effect of natural and synthetic estrogen].

This investigation was conducted to evaluate the effects of 17 beta-estradiol and 17 alpha-ethinylestradiol on prostacyclin PGI2-production in homogenates of human umbilical cord arteries and veins in the presence of exogenous arachidonic acid. The incubation of 17 beta-estradiol at 2 different concentrations (10(-8) and 10(-6) M) in the presence of arachidonic acid for various times (5 min up to 24 h) effected an increase in the production of PGI2 (measured as 6-keto-prostaglandin F1 alpha) of 36-47% in the artery and 16-21% in the vein over basal values (100%). Under the same experimental conditions with 17 alpha-ethinylestradiol we observed an increases of 30-40% in the artery and 1-18% in the vein compared with basal values. For both estrogens this was not significantly different compared with untreated samples. In our in vitro system, natural and synthetic estrogens had no clear effect on PGI2 production in homogenates of human umbilical vessels.

6-Ketoprostaglandin F1 alpha↗
PubMed1991

Distribution of immunoreactive relaxin in the genital tract and in the mammary gland of non-pregnant women.

Relaxin was determined in healthy and pathological tissue samples from mammary gland, ovary, myometrium and cervix uteri of non-pregnant women. Relaxin could be detected in all groups of tissues examined. The highest values were found in healthy ovary, the lowest concentrations in the cervix, which is known as a target organ for relaxin activity during pregnancy. Mammary parenchyma showed the highest specific activity of all healthy tissues examined. The relaxin concentration in myoma tissue is significantly higher than in healthy myometrium.

Breast↗
PubMed1989

[The hormone profile in serum and cervix secretions in the course of a menstrual cycle].

Serum and cervico-vaginal secretion were examined for LH, E2, progesterone and relaxin content throughout a cycle. Estimations were carried out using radioimmunoassays. LH, E2 and progesterone were found in markedly lower concentrations in cervical-vaginal secretion than in serum. Relaxin was detected only in cervical-vaginal secretion with the exception of one serum sample.

Adult↗
PubMed1988

Immunoreactive relaxin in human cervico-vaginal secretion.

Relaxin was measured in cervico-vaginal secretion of non-pregnant women of reproductive age using the heterologous radioimmuno-assay for porcine relaxin. It was detected in about three-quarters of the samples collected. The mean value of the 529 samplers tested was 599 pg/ml. There was a slight trend to higher relaxin values during the second week of the menstrual cycle.

Adult↗
PubMed1988

Relaxin and human chorionic gonadotropin concentrations in blood serum during the first trimester of normal and pathological pregnancy.

Relaxin and human chorionic gonadotropin (HCG) were determined in the blood serum of women during normal and pathological pregnancy in the 1st trimester. In normal pregnancy, the hormones showed similar behavior in their secretion pattern up to the 7th week with continuously increasing concentrations. Thereafter different patterns in their secretion developed. In pathological pregnancy, both relaxin and HCG concentrations were significantly lower than in undisturbed pregnancy, following an almost parallel course without peaks.

Chorionic Gonadotropin↗
PubMed1988

Relaxin deficiency in the placenta as possible cause of cervical dystocia. A case report.

In a case of cervical dystocia which had to be delivered by caesarean section, the placenta was examined for relaxin content. The placenta was processed by acidic acetone extraction and separation of the raw extract on a carboxymethylcellulose column. The activity of relaxin was estimated by means of heterologous porcine radioimmunoassay. The elution profile of the placenta extract showed significant differences to that of the placenta in normal deliveries i.e. there was no evidence of typical protein peaks with relaxin activity. It is suggested that there is possibly a causal relationship between the lack of placental relaxin and the pathological behaviour of the cervix during delivery.

Adult↗
PubMed1987

Dose response relationship of relaxin on the pubic ligament of the mouse.

In the present work, the dose-response relationship of highly purified porcine relaxin has been examined on broadening of the pubic ligament in mice. Using the method of Steinetz et al. with 7 days of oestriol priming, higher sensitivity of the pubic ligament was attained in mice with an original weight of 10 g than in those with a weight of 20 g. S-shaped curves were obtained; by increasing the relaxin doses after maximal effect had been reached a decreased action was observed. With presomen priming, a relaxin effect was established after only 2 days instead of the usual 8 days but the action was markedly less than in the Steinetz test.

Animals↗