Uterine contraction
A uterine contraction is a muscle contraction of the uterine smooth muscle.
Throughout menstrual cycle
The uterus frequently contracts throughout the entire menstrual cycle, and these contractions have been termed endometrial waves or contractile waves.[1] These appear to involve only the sub-endometrial layer of the myometrium.[1]
Follicular and luteal phase
In the early follicular phase, these contractions occur once or twice per minute and last 10–15 seconds with a low amplitude of usually 30 mmHg or less. This sub-endometrial layer is rich in estrogen and progesterone receptors.[1] The frequency increases to 3–4 per minute towards ovulation. During the luteal phase, the frequency and amplitude decrease, possibly to facilitate any implantation.
Menstruation
If implantation does not occur, the frequency remains low, but the amplitude increases dramatically to between 50 and 200 mmHg producing labor-like contractions at the time of menstruation.[1] These contractions are sometimes termed menstrual cramps,[2] although that term is often used for menstrual pain in general. These contractions may be uncomfortable or even painful, but they are generally significantly less painful than contractions during labour. Painful contractions is called dysmenorrhea.
Directionality of contractions
A shift in the myosin expression of the uterine smooth muscle has been hypothesized to avail for changes in the directions of uterine contractions that are seen during the menstrual cycle.[1]
Childbirth
A contraction refers specifically to the motion of the uterus[3] as part of the process of childbirth. Contractions, and labour in general, is one condition that releases the hormone oxytocin into the body. Contractions become longer as labour intensifies.
Prior to actual labour, women may experience Braxton Hicks contractions, sometimes known as "false labour."
Uterine contractions during childbirth can be monitored by cardiotocography, in which a device is fixated 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.[4]
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.[5]
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.[6]
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.[6]
Restoration to resting state
Uterine smooth muscle mechanisms of relaxation differ significantly from those of other human smooth muscles.[6] 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]
In orgasm
The uterus and vagina contract during female orgasm.[7]
See also
References
- ^ a b c d e f g h i j 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.
- ^ medicinenet.com > Menstrual Cramps Retrieved January 2011
- ^ Uterine+Contraction at the U.S. National Library of Medicine Medical Subject Headings (MeSH)
- ^ Tocodynamometer. By Dr. Malcolm C Brown. Copyright 2000
- ^ 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.
- ^ a b c "A Role of Stretch-Activated Potassium Currents in the Regulation of Uterine Smooth Muscle Contraction". Acta Pharmacol Sin. 32 (6): 758–764. 2011. doi:10.1038/aps.2011.62. PMC 4009969. PMID 21642947.
{{cite journal}}: Unknown parameter|authors=ignored (help) - ^ 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.
{{cite journal}}: Unknown parameter|lay-date=ignored (help); Unknown parameter|lay-source=ignored (help); Unknown parameter|lay-url=ignored (help)