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Biomedical subjects

T H Lippert

Publications and source records attributed to T H Lippert.

At least 55 records · Page 3Linked to original sources
PubMed1996

Serotonin metabolite excretion after postmenopausal estradiol therapy.

Serotonin, known for its beneficial action on mood and well-being, is also involved in cardiovascular functions. Thus the current work was undertaken to study the effect of hormone replacement therapy on serotonin turnover in postmenopausal women. Eighteen women received estradiol transdermally and 17 women estradiol valerate orally for 4 weeks. The serotonin metabolite 5-hydroxyindole acetic acid (5-HIAA) was determined in the urine before, and after 2 and 4 weeks' estradiol treatment. With both administration routes estradiol produced a significant increase in urinary 5-HIAA excretion, greatest with transdermal estradiol after 28 days of treatment. The enhancement of serotonin turnover may contribute not only to an improvement of mood and well-being but also to a cardioprotective effect of estradiol observed after hormone substitution in postmenopausal women.

Administration, Cutaneous↗
PubMed1996

Effect of 17 alpha-ethinylestradiol, levonorgestrel, 3-keto-desogestrel, and gestodene on calcium influx via voltage-gated calcium channels in human aortic smooth muscles.

The effect of the synthetic estradiol, 17 alpha-ethinylestradiol, and three progestogens on calcium influx was investigated in cell cultures of human aortic smooth muscle. Neither the synthetic estrogen nor the progestogens levonorgestrel, 3-keto-desogestrel, and gestodene showed, in the concentration range of 10(-9) to 10(-6) M, a significant effect on calcium influx both alone or in equimolar estrogen-gestagen combinations. The results indicate that these substances, commonly used in contraceptive pills, do not change vasotonus interfering with calcium homeostasis.

Aorta↗
PubMed1996

Urinary cGMP excretion after hormone replacement therapy in postmenopausal women.

It is well established that estrogens and progestogens are able to influence the vasotonus in postmenopausal women. The present study was undertaken to find out if the NO/cGMP-system is involved in this hormone action. Urinary cGMP excretion which can reflect intracellular cGMP production elicited by NO (EDRF) was investigated in 20 postmenopausal women. In an open cross-over study design norethisterone acetate was administered orally for 8 days, estradiol valerate orally for 9 days and a combination of both substances for 12 days. After all three treatment phases urinary cGMP expressed as percentage of the pretreatment value was increased at a statistically significant level. Due to high individual variations no significant differences could be found among the values after the three treatment phases. It was concluded that the NO/cGMP-system may play a role in maintaining vasotonus in postmenopausal women under hormone replacement therapy.

Administration, Oral↗
PubMed1996

-Is prevention of pre-eclampsia with low dosage aspirin possible? Critical assessment of available studies-.

The efficacy of low-dose aspirin treatment to prevent preeclampsia was assessed by reviewing studies of the available literature. 9 studies were performed examining nearly 13,000 pregnant women. Aspirin treatment compared with untreated control groups led to a significant reduction of preeclampsia in 5 small-scale studies. However, no prophylaxis could be achieved in 4 studies comprising more than 12,000 pregnant women. A assessment of low-dose aspirin treatment is difficult, since no dose-response study was performed to determine the optimal dose; the duration of treatment--beginning and end--was not defined and the drug risk for mother and child was not documented in accordance with GCP guidelines. The major problem of all studies, however, consisted in the recruitment of the patients since there are no easily performable and well-recognised screening tests available to estimate the risk of preeclampsia. In conclusion, at present no statement is possible if and under which conditions low-dose aspirin treatment will be able to prevent preeclampsia.

Aspirin↗
PubMed1996

Does melatonin affect calcium influx in human aortic smooth muscle cells and estradiol-mediated calcium antagonism?

The pineal hormone melatonin showed no effect on voltage-gated calcium channels in cultured human aortic smooth muscle cells. In combination with estradiol, which blocked calcium channels, melatonin did not antagonize the effect of estradiol. It is concluded that melatonin seems to have different effects on voltage-gated calcium channels of divergent cell types since the positive action of melatonin previously observed on rat cardiac membranes by other authors could not be seen in the present investigations with human vascular smooth muscle cells.

Adult↗
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

Hepatic hydroxylation of melatonin in the rat is induced by phenobarbital and 7,12-dimethylbenz[a]anthracene--implications for cancer etiology.

The protective function of the pineal hormone melatonin in the etiology of cancer and carcinogenic activation is increasingly well-established. Low melatonin levels seem to parallel cancer growth. The question arises as to which factors cause the depression of melatonin levels and what the direct effects are. Melatonin is known to be metabolized in the liver by hydroxylation and subsequent conjugation yielding 6-sulfatoxymelatonin as a main product. Nevertheless, the microsomal monoxygenases catalyzing the first step have been poorly investigated. To further characterize these enzymes, typical inducers of three different sub-classes, namely phenobarbital, 7,12-dimethylbenz[a]anthracene, and 17 beta-estradiol, were administered to female Fischer rats. Circadian urinary excretion patterns of melatonin and 6-sulfatoxymelatonin were determined over a 24-hour period on the third (second) day of induction. Liver homogenates were used to monitor the in vitro conversion of melatonin or 6-hydroxymelatonin to 6-sulfatoxymelatonin. Results of both approaches showed the microsomal monoxygenases catalyzing the 6-hydroxylation of melatonin to be strongly inducible by phenobarbital and to a lesser degree by the polyaromatic hydrocarbon 7,12-dimethylbenz[a]anthracene. The dramatic depletion of circulating melatonin as a result of these induction patterns and its possible implications for oncogenesis are discussed.

9,10-Dimethyl-1,2-benzanthracene↗
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

Seasonality of pineal melatonin production in the rat: possible synchronization by the geomagnetic field.

Pineal melatonin production was estimated by means of urinary 6-sulfatoxymelatonin (aMT6s) determination in two groups of female rats for 1 year each. Seasonal changes of nocturnal aMT6s excretion were found with peak levels in summer despite constant photoperiods. We hypothesize that the horizontal component H of the geomagnetic field may act as a seasonal zeitgeber because H shows a similar seasonal rhythm, and changes in the direction and intensity of H can affect pineal activity. The observed seasonal changes of pineal melatonin production stress that despite constant environmental conditions, endocrine experiments require consideration of season, neglect of which may lead to contradictory results.

Animals↗
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

Antitumor activity of the pineal gland: effect of unidentified substances versus the effect of melatonin.

There is growing evidence that the pineal gland has antineoplastic properties which, however, can only partially be attributed to its hormone melatonin. While the in vivo tumor-inhibiting activity of melatonin is established, observations on its in vitro effects have been contradictory. The effect of this substance was investigated on six human cancer cell lines and compared to the activity of a partially purified, melatonin-free low molecular weight pineal extract (UMO5R). Melatonin showed hardly any effect but UMO5R was capable of inhibiting the growth of all the six cell lines tested. It is therefore concluded that a direct inhibiting action on tumor cells is not a general physiological role of melatonin as opposed to UMO5R. It will be worthwhile to purify the yet unidentified pineal antitumor activity since it may have a considerable therapeutic potential.

Humans↗