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Results for “Progesterone--side effects”

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PubMed1977

Uterine blood flow and its distribution after chronic estrogen and progesterone administration.

The rates and distributions of uterine blood flow (UBF) were measured in conscious castrated ewes during estradiol, progesterone, and combined-hormone regimens. Supplemental progesterone decreased the magnitude of UBF observed on estradiol alone. Progesterone favored distribution of UBF to the uterine caruncles and estradiol favored distribution to the myometrium and uterine cervix. Proportionate endometrial blood flows were similar on all hormone regimens. These observations suggest that estradiol secretion may not be responsible for the definitive increase in UBF observed during ovine pregnancy.

Animals↗
PubMed1977

Human cervical mucus. II. Changes in viscoelasticity during the ovulatory menstrual cycle.

Quantitative viscoelasticity measurements were made on individual human cervical mucus samples by microrheometry. Increases in mean values for mucus spinnbarkeit, ferning, and wet weight were associated with the ovulatory phase of the menstrual cycle, while no significant differences versus time were noted for mean values for sample pH or nondialyzable dry weight. A nadir in mucus nondialyzable solids (NDS) concentration and in visoelasticity was seen at or near midcycle. Substantial, highly reproducible, variations in mucus viscoelasticity were observed when mucus from different donors was compared. When the contribution of (NDS) to viscoelasticity was minimized by data normalization or by sample reconstitution, a significant increase in viscoelasticity was associated with the ovulatory phase of the cycle, suggesting the occurrence of a relative increase in mucin concentration or a compositional change in the mucus.

Cervix Mucus↗
PubMed1977

Studies on the effects of pharmacologic doses of cortisone acetate and several nonsteroidal anti-inflammatory compounds on ovo-implantation, early pregnancy, and the deciduomal response in the rat.

Cortisone acetate (10 mg/day), alone or in combination with progesterone (4 mg/day); progesterone (4 mg/day); progesterone (4 mg/day) plus estrone (1 microng/day); indomethacin (0.75 mg/day); phenylbutazone (20 mg/day); flufenamic acid (10 mg/day); and Compound 83161 (tetrazolo less than 1,5-alpha greater than s-triazolo less than 3,4-c greater than quinoxoline) (8 mg/day and 12 mg/day) were each given to intact rats during early pregnancy (days 1 and/or 2 through day 8). Only cortisone acetate treatment caused a true delay in ovo-implantation. Both progesterone treatment beginning on day 1 and cortisone acetate treatment beginning on day 1 or 2 caused an increased postimplantation fetal death rate. Compound 83161, at doses causing signs of general toxicity (12 mg/day), caused a marginal inhibition of implantation. Treatment with indomethacin, phenylbutazone, or flufenamic acid caused some inhibition of the traumatic deciduomal response in spayed rats treated with progesterone, while treatment with cortisone acetate and Compound 83161 did not.

Animals↗
PubMed1977

The effect of intrauterine progesterone treatment on the endometrial prostaglandin F content in the rabbit.

The effect on rabbit endometrial prostaglandin F caused by progesterone delivered directly to the uterus was investigated. Four groups of animals were used in the experiment: (1) no treatment (control); (2) an empty Silastic capsule (as an intrauterine device [IUD]) was inserted in one horn and the other horn was sham-operated; (3) a Silastic capsule releasing 150 microng of progesterone/day was placed in one horn and the other horn was sham-operated; (4) a Silastic capsule releasing progesterone was placed in one horn and the opposite horn received an empty Silastic capsule. In group 1, which received no treatment, no difference was noted. In group 2, the prostaglandin content of the horn containing an empty IUD was significantly higher than that of the sham-operated horn. In group 3, the same significant difference was noted between the prostaglandin content of the IUD-containing, progesterone-treated horn and the sham-operated horn. In group 4, no significant difference was observed between the horn containing an inert IUD and that containing a progesterone-releasing device. The addition of progesterone to an IUD does not significantly affect the elevated prostaglandin content of the endometrium caused by an inert IUD.

Animals↗
PubMed1977

Mechanism of oestrogen and progesterone effects on lipid and carbohydrate metabolism: alteration in the insulin: glucagon molar ratio and hepatic enzyme activity.

As in women receiving oestrogens the administration of 17beta-oestradiol to ovariectomized female rats caused a rise in fasting plasma triglycerides and a fall in plasma glucose. Progesterone, on the other hand, had no significant effects. In the oestradiol treated rats, the portal vein basal insulin levels were slightly reduced. Oestradiol, however, had a marked suppressive effect on the alpha cells of the pancreas resulting in a greater reduction in basal glucagon and impaired glucagon response to alanine infusions. The relative insulin to glucagon (I/G) molar concentration ratio in portal vein blood was increased. Oestradiol also produced a dose dependent increase in the activity of the liver lipogenic enzymes, acetyl CoA carboxylase and fatty acid synthetase. On the other hand, the activity of the gluconeogenic rate limiting enzyme phosphoenol-pyruvate carboxykinase (PEPCK) was inhibited. The cross-over pattern of gluconeogenic intermediates confirmed inhibition of gluconeogenesis at this step, an effect which is similar to that induced by relative insulin 'excess'. Progesterone produced an increase in the portal vein insulin concentrations. Both the basal and the alanine-stimulated glucagon levels were also increased. The I/G molar ratio in portal vein blood of progesterone treated rats remained unaltered and the hepatic lipogenic and gluconeogenic enzyme activities were similar to control animals. These data suggest that insulin activity is increased relative to glucagon in the liver of oestradiol-treated rats due to the rise in portal vein I/G ratio. The changes in liver lipogenic and gluconeogenic enzymes and the alterations in fasting plasma triglycerides and glucose in response to oestrogens could be secondary to this effect.

Acetyl Coenzyme A↗
PubMed1977

Effect of progestins on glucose and lipid metabolism.

Gestamimetic amounts of progesterone enhance basal and glucose-stimulated insulin production. Contraceptive doses of synthetic progestins cause a moderate increase or no change in glucose-stimulated insulin production, depending on route of administration and species tested. Estrogens potentiate the insulinotropic effects of progesterone and the synthetic progestins. Basal serum triglyceride concentrations are generally unaffected by progesterone or 17 alpha-acetoxyprogesterone treatment but may decrease during 19-nortestosterone administration. Glucose tolerance does not change during treatment with gestamimetic doses of progesterone alone but may improve in rats and monkeys during concurrent estrogen administration. By contrast, deterioration of glucose tolerance is observed in women treated concurrently with synthetic estrogen plus 19-nortestosterone derivatives and, occasionally, with 19-nortestosterone derivatives alone. No consistent changes in glucose metabolism have been observed after treatment with 17 alpha-acetoxyprogesterone derivatives alone. The cause of the species-related differences in glucose metabolism during 19-nortestosterone treatment is obscure.

Animals↗
PubMed1975

Action of luteinizing hormone-releasing factor (lrf) in the initiation of lordosis behavior in the estrone-primed ovariectomized female rat.

In order to evaluate the precise role of luteinizing hormone-releasing factor (LRF) in mediating the onset of sexual behavior, the specificity, time-course, and dose-response relationship of LRF-facilitated lordosis behavior were determined. Ovariectomized female rats, pretreated with estrone and LRF, displayed a pattern of lordosis behavior which differed little from that produced by estrone-progesterone. Little if any lordosis behavior was observed in response to LRF alone, estrone alone, or estrone in combination with luteinizing hormone (LH), follicle-stimulating hormone (FSH), or thyrotropin-releasing factor (TRF). Furthermore, LRF-induced lordosis behavior occurred in the absence of the adrenals, thus eliminating adrenal progesterone as a factor in facilitating the appearnce of lordosis behavior. The LRF-facilitated lordosis behavior was seen 2 h after the injection of LRF and was maintained for a total of 8 h. A minimal dose of 150 ng LRF was required to initiate the first consistent appearance of lordosis behavior; the maximum response was obtained with 500 ng. It is thus suggested that LRF is not only responsible for the ovulatory discharge of LH and subsequent ovulation, but may also play a role in the initiation of the onset of mating behavior in the female rat.

Adrenal Glands↗
PubMed1976

[Mechanism of LH release with synthetic LH-RH (author's transl)].

The purpose of this study is to examine the effect of LH-RH on LH release in the baboon. Fifteen female baboons having the normal menstrual cycle were used for this study. On hundred mug of synthetic LH-RH was injected subcutaneously in both the early follicular phase and the early luteal phase. For control purposes, 1 ml of saline was injected subcutaneously in the luteal phase. Blood samples were collected by femoral vein puncture with light anesthesia under prearranged schedule and were assayed for LH-RH, LH, estrogen and progestin. The plasma level of LH-RH reached a maximum within 4 minutes after s.c. injection of 100 mug LH-RH, decreased sharply at first, and then slowly later. Fast and slow disappearance components (t1/2 = 4.7 min., 37.1 min. respectively) were observed. In the baboon given LH-RH during the luteal phase, peaks in plasma levels of LH were observed within 30 minutes and within 90 to 150 minutes after injection. A lesser pituitary response to LH-RH for LH release occurred during the follicular phase. The first peak of LH was well-correlated with the peak of plasma LH-RH but the later elevations of LH (observed within 90 to 150 minutes after LH-RH injection) were not necessarily related to the plasma level of immunoassayable LH-RH. Elevation of plasma levels of estrogen and progestin was observed wtihin 45 minutes after LH-RH injection. In saline control, the plasma level of LH was not elevated; however, plasma levels of estrogen and progestin were increased within 45 minutes after saline injection. Later elevation of plasma LH observed between 90 and 150 minutes after LH-RH injection may be due to administered LH-RH in cooperation with elevated levels of plasma estrogen and progestin. To pursue this problem, injections of estrogen and/or progesterone were performed during the early follicular phase. Injection of 600 mug of estrodiol benzoate (EB) for 3 days caused an elevation of plasma level of LH and enhanced pituitary LH responsiveness to LH-RH for LH release; however, injection of 100 mug EB for 3 days showed less effect on LH release. Injection of 10 mg of progesterone for 3 days also caused an elevation of plasma level of LH and enhanced the pituitary responsiveness to LH-RH release. Injection of both 600 mug EB and 10 mg progesterone for 3 days did not elevate plasma level of LH and showed no significant effect of LH-RH on LH release as compared to control. These results suggest that elevated levels of circulating estrogen and progestin may determine LH release and exposure of the pituitary to LH-RH is necessary for LH release. In dose and time schedule used in this study, it is inferred that estrogen and progesterone may exert their direct effect to hypothalamus on endogenous LH-RH secretion and also may exert their effect on pituitary gonadotrophs to change the sensitivity to LH-RH, i.e. these steroid hormones may be major factors in the control of gonadotropin release in the baboon.

Animals↗
PubMed1977

Progestagen effects on elicitation of aggressive behaviour in male mice.

Effects of progesterone on production of androgen-dependent aggression-eliciting pheromones were investigated. Two groups of anosmic (non-fighting) castrated mice treated with testosterone or with testosterone and progesterone, respectively, were attacked to the same degree by intact, isolated (fighting) mice while control mice (castrated only) were attacked less. The findings support the ideas that progesterone may inhibit androgen-induced aggression via a neural and not via a somatic mechanism.

Aggression↗
PubMed1976

Enzymatic responses of transplanted tumour cells towards estrogen, progesterone and testosterone.

The influence of estrogen, progesterone and testosterone on the activities of alkaline and acid phosphatases, adenosine triphosphatase and succinate dehydrogenase were determined by cytochemical methods in sarcoma 180 and Ehrlich's carcinoma cells transplanted in male and female Swiss mice. The results revealed differential effects of the sex hormones on different enzymes which seemed to depend on the type of tumour cell studied and the sex of the host mice.

Acid Phosphatase↗
PubMed1976

The mechanism of action of the copper intrauterine device.

The effects of copper ions on the binding of steroids to receptors revealed that the inhibitory effect of Cu++ was apparent at 10(-6)M, ANd the binding capacities decreased to 10% at 10(-2)M Cu++. The kinetic study demonstrated that Cu++ was a competitive inhibitor of steroid hormone-receptor binding (Ki divided by 2.7 X 10(-5)M to estrogen receptor; Ki divided by 5.1 X 10(-6)M to progesterone receptor). These results indicate that copper ions interfere at the steroid-binding site of receptor and that progesterone receptor is more affected by copper ions than is estrogen receptor. The sedimentation pattern showed the dissociation and aggregation of receptor macromolecules by copper. These phenomena may indicate the biologic inactivation of receptor. In fact, morphologically, progestational proliferation was severely inhibited and estrogenic action seemed to be inhibited. The Timm stain showed copper uptake by endometrial epithelium and superficial stromata. The copper content apparently increased in the cytoplasm of uteri bearing a copper intrauterine device, compared with controls. In vivo, the concentration of cytoplasmic copper was approximately 1.4 X 10(-6)M, which was obviously inhibitory to steroid hormone-receptor interaction. However, complete morphologic suppression of the progestational effect by copper cannot exclude the coexistence of some other mechanism in these phenomena.

Animals↗