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Results for “Progesterone--administraction and dosage”

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At least 19 recordsLinked to original sources
PubMed1977

Further studies on a new bioassay of progestational activity (traumatic deciduoma formation in immature rats).

Six synthetic steroids were tested subcutaneously in a new bio-assay for short- and long-lasting progestational activity, using traumatic deciduoma production in immature female rats. As reference standard, a daily subcutaneous dose of 0.25 mg progesterone regularly induced a distinct deciduomagenic effect. A single dose of 12.5 mg of progesterone showed a prolonged activity. Medroxyprogesterone acetate showed a distinct deciduomagenic effect at the 0.05 mg daily s.c. dose level; a distinct prolonged effect was induced with a single s.c. injection of 0.5 mg. 16alpha-Aethylprogesterone induced regularly decidual reaction at the 0.1 mg s.c. dose level, it showed prolonged activity at the 0.25 mg dose level. The daily threshold dose for chlormadinone acetate was 0.25 mg; prolonged activity was shown with 2.5 mg. The daily threshold dose for duphaston is between 0.5 mg and 1.0 mg. A single s.c. dose of as much as 20.0 mg of 17alpha- hydroxyprogesterone caproate did not have a deciduomagenic effect.

Animals↗
PubMed1979

Low-level, progestogen-releasing vaginal contraceptive devices.

Silicone rubber vaginal contraceptive devices of four different formulations, which release predetermined, controlled doses of three progestogens at four distinct levels, were designed and fabricated, and tested in 90-day clinical trials. Data obtained with 70 of the devices indicated that in vivo release rates (microgram/day +/- S.D.) for the formulations were: progesterone, 1400 +/- 30; norethindrone (two levels), 49.4 +/- 2.4, 196 +/- 21; d-norgestrel, 21.6 +/- 1.4. Clinical studies with these devices indicate that the women usually ovulate (with the exception of the high-dose norethindrone-releasing devices) while sperm penetration of the cervix was inhibited by all four fromulations, most consistently by the norgestrel-releasing devices.

Contraceptive Devices↗
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↗
PubMed1977

Postnidatory effects of luteinizing hormone releasing hormone (LHRH) in hamsters.

Whereas the administration of LHRH to pregnant hamsters has no effect during the prenidatory period, the hormone is effective in terminating pregnancy when given after implantation (days 6-10). The ED50 for pregnancy termination over this period approximates a dose of 0.35-0.4 mg b.i.d. When given to pregnant females in a second study, the effects of LHRH at this dose were completely reverse by minute doses of progesterone (30 microgram and above). Finally, administration of LHRH at 1.5 mg b.i.d., from days 6-10 was followed by daily sacrifice through day 12; bloods were sampled at autopsy for progesterone evaluation. Autopsies on days 7 and 8 showed few differences between controls and LHRH-treated hamsters, although decreased weights of the uterine/conceptus units signaled the initation of resorption. Significant LHRH-induced decreases in circulating progesterone were seen by day 9. Fetal resorption continued and was essentially complete by day 11, while progesterone levels continued depressed through the end of the study.

Animals↗
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↗
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↗
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

Disseminated intravascular coagulation induced by progesterone in the pregnant rat. Prevention by estogens.

Fatal disseminated intravascular coagulation (DIC) was induced in female rats by administration of progesterone in late pregnacy. This prevented parturition, with intrauterine fetal death 2 to 4 days past term and subsequent retention of dead fetuses. Concomitantly with or closely following the intrauterine death of their litters, a large proportion of pregnant rats died with histologically evident DIC. Administration of cortisone, heparin, or disoumarin did not prevent DIC, and xi-aminocaproic acid, acetylsalicylic acid, or an onion-rich diet tended to increase its incidence. Antibiotic regimens gave variable results, with significant decrease in DIC only with a combination of two wide-spectrum penicillins. Neomycin and polymyxin had little effect on susceptible Sprague-dawley derived rats, but polymxin caused a significant increase in DIC in a resistant strain of hooded rats. Fatal maternal DIC was completely prevented only by use of natural or synthetic estrogens concurrently with progesterone, although this did not alter the sequence of abnormally prolonged pregnacy with intrauterine fetal death and retention of dead fetuses. Potencies of estrogens varied greatly, but all compounds tested prevented DIC at adequate dosage levels. Diethylstilbestrol, the most potent drug tested, was completely protective at 1 mug daily given subcutaneously. beta-Estradiol was the most effective natural estrogen, giving complete protection with a 10-mug daily subcutaneous injection. Estrogens were much more potent by subcutaneous injection than by oral ingestion, and toxic side effects were sometimes noted with higher levels of the latter. For estrogen therapy to be effective, it was necessary to begin its use before the expected onset of DIC, and in no instance was there evidence of reversal of this process after signs of illness were observed.

Animals↗
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↗
PubMed1979

A new long-acting injectable microcapsule system for the administration of progesterone.

A long-acting injectable microcapsule system for the controlled-release systemic administration of progesterone (P4) is described. The system consists of microcapsules made of the biodegradable polymer, d,l-polylactic acid, which contain crystalline P4. Following injection, P4 is released from the microcapsules by diffusion and biodegradation of the polymer matrix. The rate of P4 release from the prototype microcapsule system in vivo is 1.3 microgram of P4/day/mg of microcapsules, and the duration of release is 30 days. Vaginal estrous cycles in rats and cyclic ovarian function in baboons were inhibited for 1 month following a single injection of P4 microcapsules. The effects of continuous progesterone therapy on reproductive function in both rats and baboons are dose-dependent. The utility of the system as a once-a-month injectable contraceptive is established in the baboon model.

Animals↗
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↗