Uterine contraction

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Uterine contractions are

uterine smooth muscle that can occur at various intensities in both the non-pregnant and pregnant uterine state. The non-pregnant uterus undergoes small, spontaneous contractions in addition to stronger, coordinated contractions during the menstrual cycle and orgasm. Throughout gestation,[1] the uterus enters a state of uterine quiescence due to various neural and hormonal changes. During this state, the uterus undergoes little to no contractions, though spontaneous contractions still occur for the uterine myocyte cells to experience hypertrophy.[1] The pregnant uterus only contracts strongly during orgasms, labour, and in the postpartum stage to return to its natural size.[2]

Throughout menstrual cycle

Uterine contractions that occur throughout the

endometrial layer of the myometrium.[3]

Follicular and luteal phase

In the early

implantation
.

Menstruation

If implantation does not occur, the frequency of contractions remains low; but at

menstrual pain in general. These contractions may be uncomfortable or even painful,[5] but they are generally significantly less painful than contractions during labour. Painful contractions are called dysmenorrhea
.

Directionality of contractions

A shift in the

uterine smooth muscle has been hypothesized as arising for changes in the directions of uterine contractions during the menstrual cycle.[3]

Labour and pregnancy

Uterine contractions are a vital part of natural

vaginal canal
during the first stage of labour.

Throughout pregnancy, the uterus experiences motor denervation, thus inhibiting spontaneous contractions. The remaining contractions are predominantly hormonally controlled. The decrease in the coordination of uterine smooth muscles cells reduces the effectiveness of contractions, causing the uterus to enters a state of uterine quiescence.[8] During the beginning of labour, contractions may initially be intermittent and irregular,[7] but will transition into a more coordinated pattern as the labour progresses.[7] This transition is governed by various myogenic, neurogenic, and hormonal factors working together.[8] As labour progresses, contractions will typically increase in frequency and intensity, which leads to a significant rise in intrauterine pressure.[7]

Otherwise, not all contractions experienced by pregnant individuals are indications of the beginning of labour. Some women experience what are commonly called Braxton Hicks contractions before their initial due date, which are characterized as “false labour." Though similar to labour uterine contractions, these contractions do not play a prominent role in cervical dilation or the progression of childbirth.

Oxytocin

The hormone oxytocin has been identified as inducing uterine contractions, and labour in general.[9] Oxytocin is produced by the body naturally and since the 1950s has also been available in synthetic pharmaceutical form.[10][11] In either form, oxytocin stimulates uterine contractions to accelerate the process of childbirth. Production and secretion of oxytocin is controlled by a positive feedback mechanism, where its initial release, either naturally or in pharmaceutical form, stimulates production and release of further oxytocin. For example, when oxytocin is released during a contraction of the uterus at the start of childbirth, this stimulates production and release of more oxytocin and an increase in the duration, intensity and frequency of contractions. This process compounds in intensity and frequency and continues until the triggering activity ceases.

Prostaglandins

The concentration of prostaglandins in the

connexin-43 expression during labor.[9]

In orgasm

Uterine and vaginal contractions usually take place during female sexual stimulation, including sexual arousal, and orgasm.[12]

Monitors

Knitted Bellyband with conductive thread and RFID chip to monitor contractions

Uterine contractions can be monitored by cardiotocography, in which a device is affixed to the skin of the mother or directly to the fetal scalp. The pressure required to flatten a section of the uterine wall correlates with the internal pressure, thereby providing an estimate of it.[13]

A type of monitoring technology under development at Drexel University embeds conductive threads in the knitted fabric of a bellyband. When the fibers stretch in response to a contraction, the threads function like an antenna, and send the signals they pick up to an embedded RFID (radio-frequency identification device) chip that reports the data.[14]

Mechanism

Resting state

The

efflux
of positive ions, resulting in a negative potential.

This resting potential undergoes rhythmic oscillations, which have been termed slow waves, and reflect intrinsic activity of

ion flux, reflecting changes in various K+ channels.[3]

Excitation-contraction

As the uterus becomes essentially denervated during gestation, it is unlikely that any coordinated nervous regulation of the myometrium is centrally orchestrated.[15]

Excitation

The excitation-contraction coupling of the uterine smooth muscle is also very similar to that of other smooth muscles in general, with intracellular increase in calcium (Ca2+) leading to contraction.

Nitric oxide (NO) is particularly effective in relaxing the myometrium and in fact has a lower inhibitory concentration 50% (Ki) in human than guinea pig or non-human primate myometrium.[15]

Restoration to resting state

Uterine smooth muscle mechanisms of relaxation differ significantly from those of other human smooth muscles.[15] Removal of Ca2+ after contraction induces relaxation of the smooth muscle, and restores the molecular structure of the sarcoplasmic reticulum for the next contractile stimulus.[3]

Measuring uterine contractility ex vivo

Ethically donated human uterine tissues can be used to measure uterine contractility ex vivo. In these experiments, sections of myometrium are set up in an organ bath system that to measure changes in isometric force production. Following functional checks to ensure the tissue is physiologically active, compounds can be added to the organ bath in increasing concentrations to create a cumulative concentration-response curve (CCRC).

A key advantage of measuring uterine contractility ex vivo is the ability to eliminate species differences. For example, while magnesium reduces myometrial contractility in

clinical studies.[16] And while the peptide hormone relaxin has been shown to inhibit uterine contractility in rats, mice, and pigs, it does not prevent uterine contractility in humans.[17]

See also

References

  1. ^
    PMID 37164494
    . Retrieved 17 March 2024.
  2. S2CID 35342557
    .
  3. ^
    PMID 20551073
    .
  4. ^ medicinenet.com > Menstrual Cramps Retrieved January 2011
  5. ^
    ISBN 978-0-323-47912-7
    , retrieved 2022-09-28
  6. ^ Uterine Contraction. U.S. National Library of Medicine Medical Subject Headings.
  7. ^
    ISBN 978-0-323-32108-2
    .
  8. ^ a b Jain, V.; Saade, G. R.; Garfield, R. E. (1999). Uterine contraction. Encyclopedia of Reproduction. 4. 932-942.
  9. ^
    ISBN 978-0-323-32108-2
    . Retrieved 2022-09-28.
  10. doi:10.1021/ja01115a553
    .
  11. doi:10.1021/ja01641a004
    .
  12. PMID 21797981
    .
  13. ^ Tocodynamometer. Dr. Malcolm C Brown. Copyright 2000
  14. ^ Reyes, Juliana (August 21, 2014). "Drexel's wearable-tech lab is making 'a radio out of fabric' for pregnant women". Technically Philly. Retrieved 10 May 2017.
  15. ^
    PMID 21642947
    .
  16. ISBN 978-0-12-386007-1
    , retrieved 2022-09-28
  17. ^ "Encyclopedia of Reproduction | ScienceDirect". www.sciencedirect.com. Retrieved 2022-09-28.
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