Effects of the Prostaglandins on the Uterus

Bygdeman, M.; Bremme, Katarina; Gillespie, Arnold; Lundström, V.

doi:10.3109/00016347909157787

Cited by 34 publications

(6 citation statements)

References 16 publications

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“…In the normal menstrual cycle, prostaglandin concentrations rise to a peak at midcycle, and then decline after ovulation (Vijayakumar and Walters, 1981). During the 1960s and 1970s, several authors suggested that prostaglandins increase UC at mid-cycle (Bygdeman et al, 1979;Eliasson and Posse, 1960;Martin et al, 1978), promoting rapid sperm transport to the Fallopian tubes. As seminal plasma contains prostaglandins (Robertson, 2005), it could provide its own transport via UC.…”

Section: Endocrine Effectsmentioning

confidence: 99%

Uterine peristalsis and fertility: current knowledge and future perspectives: a review and meta-analysis

Kuijsters

Methorst

Kortenhorst

et al. 2017

Reproductive BioMedicine Online

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Although uterine contractions in the non-pregnant uterus have been studied extensively, the knowledge gained has not been used in general fertility treatment work-up. In this review paper, we provide an overview of the current knowledge on uterine peristalsis (UP), based on the available literature. This literature shows that UP influences pregnancy chances in both natural and artificial cycles. Although the physiological background of these contractions is not completely clear, we know that several factors can be of influence, like uterine pathologies and hormones. Several options to alter pregnancy outcome by interfering with uterine contractions have been studied. Our meta-analysis on therapeutic options shows positive results of progesterone at time of embryo transfer in IVF cycles or prostaglandins at time of intrauterine insemination, although the quality of evidence is low. These therapies are probably most beneficial in selected groups of patients with abnormal contraction patterns. The introduction of an objective and user-friendly UP measuring tool suitable for use in daily practice would make it possible to identify and monitor these patients. We suggest that future research should focus on the physiology of initiation of UP and on the development of an effective standard measuring tool.

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Section: Endocrine Effectsmentioning

confidence: 99%

Uterine peristalsis and fertility: current knowledge and future perspectives: a review and meta-analysis

Kuijsters

Methorst

Kortenhorst

et al. 2017

Reproductive BioMedicine Online

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“…In nonpregnant uterus, PG� may cause relaxation. In dys menorrheic subjects, PG� has been shown to decrease myometrial activity and relieve pain (120). If a high PGF2a: PG� ratio is an important determi nant of dysmenorrhea, then PG synthetase inhibitors that have a preferen tial effect on PGF2a synthesis would be superior to those that do not exhibit this preferential action as therapeutic agents for dysmenorrhea.…”

Section: General Pharmacologic Considerationsmentioning

confidence: 99%

Prostaglandins and Nonsteroidal Antiinflammatory Drugs in Dysmenorrhea

Çhan¹

1983

Annu. Rev. Pharmacol. Toxicol.

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INTRODUCTIONDysmenorrhea, commonly known as menstrual pain or cramps, is classifi ed into primary and secondary dysmenorrhea. Generally, primary dysmenorr hea has its inception at the onset of or soon after menarche and characteris tically has no identifiable macroscopical pathology. In contrast, secondary dysmenorrhea usually has its onset in adulthood and is associated with specific pelvic pathology. Some of the causes of secondary dysmenorrhea are endometriosis, uterine polyps, pelvic inflamm atory diseases, uterogeni tal anatomical anomaly, and intrauterine device. Primary dysmenorrhea is by far the more prevalent form.The incidence and prevalence of primary dysmenorrhea have not been established, but it has been estimated that as many as 50% of women of reproductive age, particularly nulliparas, suffer from dysmenorrhea at one time or other. In approximately 10% of these dysmenorrheic subjects, the symptoms are disabling enough to cause incapacitation for one to two days a month (1-4). Primary dysmenorrhea is the most common gynecologic complaint. Because of its cyclic recurring nature, the medical and socioeco nomic impact of dysmenorrhea is enormous. It is the greatest single cause of lost work hours and school days among women (5-8), with more than 140 million work hours estimated to be lost annually (4). With increasing numbers of women entering the work force, dysmenorrhea may cause an even greater economic loss to society. 131Annu. Rev. Pharmacol. Toxicol. 1983.23:131-149. Downloaded from www.annualreviews.org Access provided by University of California -Davis on 02/03/15. For personal use only. Quick links to online content Further ANNUAL REVIEWS 132 CHAN Despite the prevalence of dysmenorrhea, until very recently, medicine has made very little headway either toward the understanding of the patho physiology of dysmenorrhea or the discovery of a specifi c and effective therapy for this female malady. The introduction of oral contraceptives in the 19608 marked the advent of the first effective therapeutic agent for the treatment of primary dysmenorrhea. Oral contraceptives, however, are not specific agents for dysmenorrhea. Until that time, treatments for dys menorrhea were primarily symptomatic, involving strong analgesics, an tidepressants, alcohol, and a variety of home remedies. These therapeutic approaches have not been successful, because of either lack of efficacy or unacceptable side effects. The first rational therapy for dySmenorrhea ap peared on the medical scene as late as the mid 19708, when the relationship between prostaglandin (pG) and dysmenorrhea was recognized and the newer nonsteroidal anti-in1lamm atory drugs (NSAIDs) with PG synthetase inhibitory activity were being introduced to the general medical practice.This review focuses on the etiologic role of PO in primary dysmenorrhea and therapeutic suppression of uterine PG production as a specifi c therapy for dysmenorrhea. PATHOPHYSIOLOGY OF PRIMARY DYSMENORRHEAMany theories have been proposed for the cause of dysmenorrhea. These inc...

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“…For example, PGE, and PGFza have opposing vascular effects causing vasodilatation and vasoconstriction respectively (Malik & McGiff 1976). While PGF,, administration stimulates uterine contractility during all phases of the menstrual cycle, PGE, may inhibit myometrial contractility during menstruation and stimulate it during the proliferative and luteal phases (Bygdeman et al 1979).…”

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confidence: 99%

Prostaglandins in menstrual fluid in menorrhagia and dysmenorrhoea

Rees

Anderson

Demers

et al. 1984

BJOG

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Summary. Menstrual fluid was collected in vaginal cups inserted for 2 h during the first 2 days of menstruation and menstrual serum concentrations of prostaglandins PGF2α and PGE2 were measured by radio‐immunoassay. In 16 women from whom menstrual fluid was collected on both days, PGF2α and PGE2 concentrations were significantly higher on day 1 than on day 2. The highest concentrations of PGF 2α and PGE2 were found in dysmenorrhoeic women on day 1. In non‐dysmenorrhoeic women, the amount of PGF2α and PGE2 collected in 2 h correlated directly with total menstrual blood loss. There was no statistically significant difference in the amount of prostaglandins collected in 2 h in pain‐free menorrhagic women and dysmenorrhoeic women with normal loss. There was also no significant 9‐ketoreductase or 9‐hydroxydehydro‐genase activity present in menstrual fluid which could suggest PGE2 to PGF2α interconversion.

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Effects of the Prostaglandins on the Uterus

Cited by 34 publications

References 16 publications

Uterine peristalsis and fertility: current knowledge and future perspectives: a review and meta-analysis

Uterine peristalsis and fertility: current knowledge and future perspectives: a review and meta-analysis

Prostaglandins and Nonsteroidal Antiinflammatory Drugs in Dysmenorrhea

Prostaglandins in menstrual fluid in menorrhagia and dysmenorrhoea

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