| Myometrium | |
|---|---|
Uterus and uterine tubes (myometrium labeled at center right) | |
Histology of myometrium | |
| Details | |
| Location | Uterus |
| Identifiers | |
| Latin | tunica muscularis |
| MeSH | D009215 |
| TA98 | A09.1.03.025 |
| TA2 | 3520 |
| FMA | 17743 |
| Anatomical terminology | |
Themyometrium is the middle layer of theuterine wall, consisting mainly ofuterine smooth muscle cells (also calleduterine myocytes[1]) but also of supporting stromal and vascular tissue.[2] Its main function is to induceuterine contractions.
The myometrium is located between theendometrium (the inner layer of the uterine wall) and the serosa orperimetrium (the outer uterine layer).
The myometrium can be divided into three layers:
The junctional layer is probably capable ofperistaltic andanti-peristaltic activity. The "circle and longitudinal" layout is similar to themuscular layer of the intestines.[1]
It is generally believed that the junctional layer derives from theMüllerian duct,[1] or more specifically themesenchyme surrounding the duct.[5] In 2022, it was found that theWoffian duct's mesenchyme also migrates to contribute. There is an obvious partitioning: the mesometrial side, derived from the Woffian, has more glands. Accordingly, implantation occurs on the antimesometrial side, while placentation happens on the mesometrial side.[6] It is unknown what the other layers develop from.[1]
The myometrium contains a "side population" of stem cells. They are presumably what allows the myometrium to grow during pregnancy.[7]
The molecular structure of thesmooth muscle of myometrium is very similar to that of smooth muscle in other sites of the body, withmyosin andactin being the predominant proteins.[1] In uterine smooth muscle, there is approximately 6-fold more actin than myosin.[1] A shift in the myosin expression of the uterine smooth muscle may be responsible for changes in the directions of uterine contractions during the menstrual cycle.[1]
The myometrium stretches (the smooth muscle cells expand in both size and number[8]) duringpregnancy to allow for the uterus to become several times its non-gravid size, and contracts in a coordinated fashion, via a positive feedback effect on the "Ferguson reflex", during the process oflabor. Afterdelivery, the myometrium contracts to expel theplacenta, and crisscrossing fibres of middle layer compress the blood vessels to minimize blood loss. A positive benefit to early breastfeeding is a stimulation of this reflex to reduce further blood loss and facilitate a swift return to prepregnancy uterine and abdominal muscle tone.
Uterine smooth muscle has a phasic pattern, shifting between a contractile pattern and maintenance of a resting tone with discrete, intermittent contractions of varying frequency, amplitude and duration.[1]
As noted for the macrostructure of uterine smooth muscle, the junctional layer appears to be capable of bothperistaltic andanti-peristaltic activity.[1]
Theresting membrane potential (Vrest) of uterine smooth muscle has been recorded to be between -35 and -80mV.[1] As with the resting membrane potential of other cell types, it is maintained by aNa+/K+ pump that causes a higher concentration ofNa+ ions in the extracellular space than in the intracellular space, and a higher concentration ofK+ ions in theintracellular space than in the extracellular space. Subsequently, havingK+ channels open to a higher degree thanNa+ channels results in an overallefflux of positive ions, resulting in a negative potential.
This resting potential undergoes rhythmic oscillations, which have been termedslow waves, and reflect intrinsic activity ofslow wave potentials.[1] These slow waves are caused by changes in the distribution ofCa2+, Na+, K+ andCl− 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 inion flux, reflecting changes in various K+ channels.[1]
Theexcitation-contraction coupling of uterine smooth muscle is also very similar to that of othersmooth muscle in general, with intracellular increase incalcium (Ca2+) leading to contraction.
Removal of Ca2+ after contraction induces relaxation of the smooth muscle, and restores the molecular structure of thesarcoplasmic reticulum for the next contractile stimulus.[1]