The main hormones involved include estrogen, progesterone and oxytocin. Oxytocin is one of the most studied hormones involved in uterine contractions. It decreases the flow of Ca2+ by inhibiting Ca2+/ATPase from the myometric cell membrane, which pumps calcium from the inside into the extracellular space, and increases the influx of Ca2+, as well as the release of Ca2+ from the SR via the IICR. Studies suggest that the increased ratio of estrogen to progesterone that occurs before the start of labor leads to an increased number of oxytocin receptors in the uterus. [14] Many animal studies also show an increase in the concentration of oxytocin before labour; However, there is little evidence of this phenomenon in men due to technical difficulties in determining oxytocin levels in working women. [15] The resting membrane potential (Vrest) of smooth uterine muscles is between −35 and −80 mV. [1] As with the resting membrane potential of other cell types, it is maintained by a Na+/K+ pump, which 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, a higher aperture of K+ channels than Na+ channels leads to a total flow of positive ions, resulting in a negative potential. Oxytocin: The process begins with the hypothalamus, especially the paraventricular and supraoptic nuclei. These nuclei produce and secrete oxytocin, the main contribution being the paraventricular nucleus.
Oxytocin then enters the posterior pituitary gland through the hypothalamic-pituitary tract. Once oxytocin arrives in the posterior pituitary gland, it then accesses the systemic blood supply that the oxytocin molecule provides to oxytocin receptors on myometric cells. Uterine epithelial clothing also makes oxytocin during pregnancy, where it acts both autocrine and paracrine. [16] [17] The positive feedback mechanism of oxytocin further catalyzes the onset of labour. [15] [18] [19]. These receptors are class 1-G rhodopsin proteins that pair with phospholipase C (PLC), which then activates inositol triphosphate (IP3) and diacylglycerol (DAG). Activated IP3 mobilizes calcium from the sarcoplasmic reticulum, which then binds to myosin`s light-chain kinases, resulting in smooth muscle contraction. [15] Cells communicate with each other via connections called gap junctions, which increase towards the end of pregnancy to help with synchronous contractions. The amount of actin and myosin present in myocytes increases during pregnancy as the uterus enlarges. Deposits of phosphocreatine, glycogen and fatty acids are increased to provide energy for contractions. Blood flow to the uterus during pregnancy increases in sync with the increasing need for blood flow, but late to the end of pregnancy. Prostaglandins also play a role in uterine contractions after the birth of the fetus.
Meanwhile, also known as stage 3 labor, the placenta secretes prostaglandins, which leads to their detachment from the endometrial cavity. [13] Contractions during this period also minimize postpartum bleeding. The absence of contractions during this period can occur due to uterine atony. If implantation does not take place, the frequency of contractions remains low; but with menstruation, the intensity increases significantly between 50 and 200 mmHg, creating labor-like contractions. [1] These contractions are sometimes called menstrual cramps,[2] although this term is also used for menstrual pain in general. These contractions can be uncomfortable or even painful, but they are usually much less painful than contractions during labor. Painful contractions are called dysmenorrhea. The myosin present in these cells is classified as IBD. It is a hexamer molecule composed of two heavy myosin chains (MHC) and two pairs of myosin light chains (MLC). It forms three basic domains.
The “head” area consists of the N-terminal spherical end of the MHC protruding laterally from the filament. It has the actin binding region as well as the ATP hydrolysis site, which provides the energy needed for contraction. This is converted into greater movement due to the stiff “neck domain” at the C-terminal end of the motor area [1]. The domain of the “neck” is also the place where the lights of the myosin fairies bind in a non-covalent way. The “tail” zone consists of the C-terminal ends of the heavy myosin chains, which are intertwined in a spiral stem α and form the main components of the thick filaments of myocytes. The main function of uterine contractions is to expel the fetus from the uterine cavity. However, contractions also play a vital role in minimizing postpartum bleeding. Knowledge of the normal physiology of uterine contractions also allows clinicians to better distinguish between the actual onset of labor and prodromal labor, also known as Braxton Hicks contractions. Braxton Hicks contractions occur sporadically and do not increase in strength. They are irregular in duration, frequency and intensity, are unpredictable and non-rhythmic, and are more uncomfortable than painful. True labor consists of contractions at regular intervals. As labor progresses, these contractions become stronger and the time between each contraction decreases.
The first stage of labor is divided into two phases, which are defined by the degree of cervical dilation. The latent phase is during dilation from 0 to 6 cm, while the active phase begins from 6 cm to the complete cervical dilation of 10 cm. The second phase of labor begins with a cervical expansion of 10 cm and ends with the birth of the baby. The third stage of labor begins when the fetus is delivered and ends with the delivery of the placenta. Uterine contractions during childbirth can be monitored by cardiotocography, in which a device is attached to the mother`s skin or directly to the fetus` scalp. The pressure required to flatten a section of the uterine wall correlates with the internal pressure, thus providing an estimate of it. [6] The interaction of uterine agonists with GPCR on the plasma membrane of the myocyte leads to a chain of events that ultimately cause the release of IP-IPR-mediated Ca from the sarcoplasmic reticulum. This further increased the concentration of calcium in the cytosol as well as the tension of the plasma membrane. Another process that causes the action potential to spread is the calcium positive feedback mechanism, known as Ca-induced Ca release (CICR), where an increase in intracellular calcium concentration stimulates the opening of other Ca channels. Perhaps the least understood is the Ca entry path operated by blind (SOCE). When the intracellular reserves of Ca in the SR are emptied, a “calcium influx factor” (CIF) is released, which causes the plasma membrane to allow the influx of extracellular Ca. Lipid rafts, called “caveolae”, which are stabilized by a scaffolding protein, caveolin, present on the plasma membrane of myocytes, are also involved in signal transduction and excitability of myocytes.
Understanding the physiology of uterine contractions allows doctors to use targeted therapy for induction and cessation of labor. Drugs commonly used to induce labor are oxytocin, misoprostol and dinoprostone. Because uterine contractions work twice to minimize postpartum bleeding, these are the same drugs used to treat postpartum bleeding. Carboprost, an analogue of PGF2a, is an additional drug used to treat postpartum bleeding that is not used for induction of labor. It was thought that there was a change in the expression of myosin from the smooth muscles of the uterus for changes in the directions of uterine contractions during the menstrual cycle. [1] The smooth muscles of the myometrium consist of thick (myosin) and thin (actin) filaments that slide over each other and thus lead to the contractile force of uterine contractions. The myometrium also has pacemaker cells; Electrical activity is distributed by lacunar junctions between myometric cells. An increase in the intracellular concentration of calcium due to the influx via the sarcolemma and / or the release of internal calcium reserves leads to contractions. Hormones and neurotransmitters can also regulate uterine activity through the entry induced by calcium agonists or other ions through receptor-controlled channels and the release of calcium stored inside.75 Does the pelvis appear to be sufficient for the infant? A delay in the active phase indicates either an insufficient effort of contraction of the uterus to enlarge the cervix, or a mechanical obstruction of childbirth. Obviously, this is a critical issue, because therapeutic alternatives are very different. If the pelvis is clinically small and/or the fetus is large and labor seems severe (e.B.
intense uterine contractions that occur every 2 minutes), the choice is caesarean section. If the fetopelvevian relationship is favorable to vaginal delivery and contractions are rare, the choice is intravenous oxytocin, amniotomy, or both. .