Difference between revisions of "Uterine Contraction - Anatomy & Physiology"
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'''''Brachystasis''''' | '''''Brachystasis''''' | ||
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* Myometrial cells contract and shorten, but do not regain their original length upon relaxation. | * Myometrial cells contract and shorten, but do not regain their original length upon relaxation. | ||
* Reduces the uterine volume and causes retraction of the [[Female_Reproductive_Tract_-The_Uterus_-_Anatomy_%26_Physiology|lower uterine segment]] and the [[Female_Reproductive_Tract_-The_Cervix_-_Anatomy_%26_Physiology|cervix]] to create a '''birth canal'''. | * Reduces the uterine volume and causes retraction of the [[Female_Reproductive_Tract_-The_Uterus_-_Anatomy_%26_Physiology|lower uterine segment]] and the [[Female_Reproductive_Tract_-The_Cervix_-_Anatomy_%26_Physiology|cervix]] to create a '''birth canal'''. | ||
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*The junction between these segments is the retraction ring. | *The junction between these segments is the retraction ring. | ||
* Palpation of the retraction ring is used as an indicator of progression through labour. | * Palpation of the retraction ring is used as an indicator of progression through labour. | ||
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| + | '''''Endocrine Control''''' | ||
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| + | Two hormones directly regulate myometrial contractions: | ||
| + | * '''[[Endocrine_System_-_Pituitary_Gland_-_Anatomy_%26_Physiology#Oxytocin|Oxytocin]]''': from the posterior pituitary gland (not the corpus luteum) lowers the excitation threshold of muscle cells to increase the likelihood of action potential firing. Oxytocin also stimulates prostaglandin release. | ||
| + | ** The uterine Oxytocin receptor is a G protein coupled receptor with a Gαq subinit. Thus the signalling pathway is via a calcium second messenger. Hence prostaglandin and oxytocin are complementory in action. | ||
| + | * '''Prostaglandins''': Stimulate liberation of calcium from intracellular stores to cause the rise in intracellular calcium concentration required for myometrial contraction. | ||
Revision as of 07:45, 8 July 2008
Myometrium consists of:
- Non-striated smooth muscle fibres
- Nerves, Blood and Lymph
- During pregnancy, Oestrogens stimulate muscle cell hypertrophy.
- Myometrial cells behave as a functional syncytium, being electrically coupled via specialised regions of contact known as gap junctions/nexi.
- The combination of the above factors allows strong, coordinated myometrial contraction.
- Excitation of smooth muscle depends on alteration in membrane potential. Myometrial cells must be depolarised (-50mV) to achive contraction.
- Spontaneous depolarizing pacemaker potentials occur. If the magnitude of these exceeds the critical threshold, a burst of action potentials will fire.
- This causes calcium influx from endoplasmic reticular stores and extracellular fluid.
- Intracellular calcium binds to regulatory sites on actin and myosin, allowing expression of ATPase, thus causing contraction.
- Uterine contractions increase in both frequency and amplitude during labour. This causes an increase in uterine pressure from 10mmHg to 50-100mmHg.
Brachystasis
- Myometrial cells contract and shorten, but do not regain their original length upon relaxation.
- Reduces the uterine volume and causes retraction of the lower uterine segment and the cervix to create a birth canal.
Retraction Ring
- The Uterus is divided into two segments:
- Upper segment: contractile
- Lower segment: passive
- The junction between these segments is the retraction ring.
- Palpation of the retraction ring is used as an indicator of progression through labour.
Endocrine Control
Two hormones directly regulate myometrial contractions:
- Oxytocin: from the posterior pituitary gland (not the corpus luteum) lowers the excitation threshold of muscle cells to increase the likelihood of action potential firing. Oxytocin also stimulates prostaglandin release.
- The uterine Oxytocin receptor is a G protein coupled receptor with a Gαq subinit. Thus the signalling pathway is via a calcium second messenger. Hence prostaglandin and oxytocin are complementory in action.
- Prostaglandins: Stimulate liberation of calcium from intracellular stores to cause the rise in intracellular calcium concentration required for myometrial contraction.