Uterine contraction

Uterine contractions are muscle contractions of the uterine smooth muscle that occur during the menstrual cycle and labour. Uterine contractions occur throughout the menstrual cycle in the non-pregnant state and throughout gestation.[1]

Throughout menstrual cycle

Uterine contractions that occur throughout the menstrual cycle, also termed endometrial waves or contractile waves,[1] appear to involve only the sub-endometrial layer of the myometrium.[1]

Follicular and luteal phase

In the early follicular phase, uterine contractions in the non-pregnant woman occur 1—2 times per minute and last 10–15 seconds with a low intensity of usually 30 mmHg or less. This sub-endometrial layer is rich in estrogen and progesterone receptors.[1] The frequency of contractions increases to 3–4 per minute towards ovulation. During the luteal phase, the frequency and intensity decrease, possibly to facilitate any implantation.

Menstruation

If implantation does not occur, the frequency of contractions remains low; but at menstruation the intensity increases dramatically to between 50 and 200 mmHg producing labor-like contractions.[1] These contractions are sometimes termed menstrual cramps,[2] although that term is also used for menstrual pain in general. These contractions may be uncomfortable or even painful,[3] but they are generally significantly less painful than contractions during labour. Painful contractions are called dysmenorrhea.

Directionality of contractions

A shift in the myosin expression of the uterine smooth muscle has been hypothesized as arising for changes in the directions of uterine contractions during the menstrual cycle.[1]

Labour

Uterine contractions are part of the process of natural childbirth[4] (i.e., not by Caesarean section). During labor, uterine contractions changes from episodic and uncoordinated to highly coordinated.[5] This change typically occurs at night, suggesting neural control, and significantly increases intrauterine pressure.[5] Some women may experience contractions before labour is due. These are Braxton Hicks contractions, which are sometimes referred to as "false labour."

Oxytocin

The hormone oxytocin has been identified as inducing uterine contractions, and labour in general.[5] Oxytocin is produced by the body naturally and since the 1950s has also been available in synthetic pharmaceutical form.[6][7] 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 blood plasma and amniotic fluid increases during labor.[3] These inflammatory mediators encourage myometrial contractions to induce labor.[3] Prostaglandins are also related to the changes in gap junction formation and connexin-43 expression during labor.[5]

In orgasm

Uterine and vaginal contractions usually take place during female sexual stimulation, including sexual arousal, and orgasm.[8]

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.[9]

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.[10]

Mechanism

Resting state

The resting membrane potential (Vrest) of uterine smooth muscle has been recorded to be between −35 and −80 mV.[1] As with the resting membrane potential of other cell types, it is maintained by a Na+/K+ pump that causes a higher concentration of Na+ ions in the extracellular space than in the intracellular space, and a higher concentration of K+ ions in the intracellular space than in the extracellular space. Subsequently, having K+ channels open to a higher degree than Na+ channels results in an overall 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 slow wave potentials.[1] These slow waves are caused by changes in the distribution of Ca2+, Na+, K+ and Cl− ions between the intracellular and extracellular spaces, which, in turn, reflects the permeability of the plasma membrane to each of those ions.[1] K+ is the major ion responsible for such changes in ion flux, reflecting changes in various K+ channels.[1]

Excitation-contraction

As the uterus becomes essentially denervated during gestation, it is unlikely that any coordinated nervous regulation of the myometrium is centrally orchestrated.[11]

Excitation

The excitation-contraction coupling of uterine smooth muscle is also very similar to that of other smooth muscle 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.[11]

Restoration to resting state

Uterine smooth muscle mechanisms of relaxation differ significantly from those of other human smooth muscles.[11] 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.[1]

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 animal studies and in vitro, it does not demonstrate the same effect in clinical studies.[12] 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.[13]

See also

References
  1. Aguilar, H. N.; Mitchell, S.; Knoll, A. H.; Yuan, X. (2010). "Physiological pathways and molecular mechanisms regulating uterine contractility". Human Reproduction Update. 16 (6): 725–744. doi:10.1093/humupd/dmq016. PMID 20551073.
  2. medicinenet.com > Menstrual Cramps Retrieved January 2011
  3. Porter, Misty Blanchette; Goldstein, Steven (2019-01-01), Strauss, Jerome F.; Barbieri, Robert L. (eds.), "Chapter 35 - Pelvic Imaging in Reproductive Endocrinology", Yen and Jaffe's Reproductive Endocrinology (Eighth Edition), Philadelphia: Elsevier, pp. 916–961.e5, ISBN 978-0-323-47912-7, retrieved 2022-09-28
  4. Uterine+Contraction at the U.S. National Library of Medicine Medical Subject Headings (MeSH)
  5. Niebyl, Jennifer R.; Simpson, Joe Leigh; Galan, Henry L. (2016). Obstetrics: Normal and Problem Pregnancies | ScienceDirect. ISBN 978-0-323-32108-2. Retrieved 2022-09-28.
  6. du Vigneaud V, Ressler C, Swan JM, Roberts CW, Katsoyannis PG, Gordon S (1953). "The synthesis of an octapeptide amide with the hormonal activity of oxytocin". J. Am. Chem. Soc. 75 (19): 4879–80. doi:10.1021/ja01115a553.
  7. du Vigneaud V, Ressler C, Swan JM, Roberts CW, Katsoyannis PG (June 1954). "The synthesis of oxytocin". J. Am. Chem. Soc. 76 (12): 3115–21. doi:10.1021/ja01641a004.
  8. Komisaruk BR, Wise N, Frangos E, Liu WC, Allen K, Brody S (2011). "Women's Clitoris, Vagina, and Cervix Mapped on the Sensory Cortex: fMRI Evidence". The Journal of Sexual Medicine. 8 (10): 2822–2830. doi:10.1111/j.1743-6109.2011.02388.x. PMC 3186818. PMID 21797981.
  9. Tocodynamometer. Dr. Malcolm C Brown. Copyright 2000
  10. 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.
  11. Iain L O Buxton; Nathanael Heyman; Yi-ying Wu; Scott Barnett; Craig Ulrich (2011). "A Role of Stretch-Activated Potassium Currents in the Regulation of Uterine Smooth Muscle Contraction". Acta Pharmacol Sin. 32 (6): 758–764. doi:10.1038/aps.2011.62. PMC 4009969. PMID 21642947.
  12. Cuppett, Courtney D.; Caritis, Steve N. (2013-01-01), Mattison, Donald R. (ed.), "19 - Uterine Contraction Agents and Tocolytics", Clinical Pharmacology During Pregnancy, Academic Press, pp. 307–330, ISBN 978-0-12-386007-1, retrieved 2022-09-28
  13. "Encyclopedia of Reproduction | ScienceDirect". www.sciencedirect.com. Retrieved 2022-09-28.
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