الفهرس 
Indications for IolOnly 14 pages are availabe for public view
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Abstract
of labor is one of the most common interventions
practiced in modern obstetrics. In the developed world, the ability to
induce labor has contributed to the reduction in maternal and perinatal
mortality and morbidity.
Labour induction may be indicated by medical or obstetrical
complications of pregnancy or may be requested or chosen for nonmedical
or social reasons.
In the first days of pregnancy, CRH suppresses the mother‘s immune
system, preventing the mother‘s body from attacking the fetus. Later,
CRH helps regulate the blood flow between the placenta and the fetus.
CRH may also help the fetal organs mature, and it appears influence the
timing of birth.
However, high cortisol levels in early pregnancy pose special risks.
Elevated cortisol is associated with an increased risk of early miscarriage.
In the last three weeks of gestation, CRH levels climb even higher.
At the same time, CRH-binding proteins diminish. Suddenly, large
quantities of CRH become available and biologically active and this lead
to major spike in cortisol levels. In the last weeks before birth, cortisol
levels are two to three times higher than normal and these levels are high.
CRH levels in plasma rise exponentially in human pregnancy.
However, this increase is more rapid in women who deliver preterm and
slower in women who deliver postterm , compared to women who deliver
at term. This rise begins early in pregnancy (16–20 weeks) and provides
evidence that placenta acts through CRH as a ―clock‖ that controls the
length of pregnancy.
Corticotrophin-releasing hormone (CRH) is master stress hormone
triggers the release of glucocorticoid stress hormones, such as cortisol at
the time of stress. so severe stress is bad for pregnancy and stress
hormones are to blame. When stress hormone levels run very high,
women are less likely to conceive and more likely to miscarry.
Placental CRH stimulates adrenocorticotropic hormone (ACTH)
production from the fetal pituitary. ACTH stimulates fetal adrenals to
produce dehydroepiandrosterone (DHEA), dehydroepiandrosteronesulphate
(DHEA-S), and cortisol. Fetal adrenal DHEA is metabolized to
estrogens in the placenta that favor parturition. Cortisol produced by fetal
adrenals acts on fetal lungs and produce surfactant protein A (SP-A) that
activates inflammatory signals in the uterus, which consequently enhance
myometrial contractility.