onset and endocrine control of Parturition.docx

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Seminar on
Onset and Endocrine control of Parturition
Submitted by
Ms. Dharti B. Bandarwar
M.SC.
In
Zoology
Special group
Mammalian Reproductive Physiology
(2022 – 2023)
Guided By
Dr. Archana A. Nerkar
Professor and Head, Department of Zoology
Govt. Institute of Science
[An Autonomous institute of Gov. of Maharashtra], Nagpur

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Govt. INSTITUTE OF SCIENCE, NAGPUR
CERTIFICATE
This is to certify that, Dharti Baleshwar Bandarwar
M.Sc. Sem IlI (Zoology) has prepare and submitted her seminar report on
Topic:-“Onset and Endocrine Control of Parturition” under the supervision
of Dr. Archana A. Nerkar Professor, and Head Department of Zoology as per
curriculum of Rashtrasant Tukdoji Maharaj Nagpur University for the award of
degree of Master of science in Zoology.
Seminar guide-
Dr. Archana A. Nerkar Dr. Archana A. Nerkar
Professor and Head Professor and Head
Department of Zoology Department of Zoology
Date-
Place- Nagpur

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ACKNOWLEDGEMENT
I wish to express my deep regards to Dr. Anjali M. Rahatgaonkar,
Director of Institute of science, Nagpur for providing the facilities for our studies.
I am heartily thankful to Dr. Archana Nerkar, Head, Department of
Zoology, for her constant encouragement and support for the Seminar work.
I wish to give my sincere thanks to Co-Guide Aasiya Syed for her
guidance and co-operation during the preparation of the Seminar topic.
Lastly, I thank the person who helped me in directing the information
mentioned in this Seminar. I am really thankful to all my professors and friends
for the valuable co-operation, Moral support and constant encouragement during
preparation of my Seminar.
Date-
Place- Nagpur
Ms. Dharti B. Bandarwar
M.Sc. Zoology [SEM-IV]

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CONTENTS
 Introduction
 Hormonal Factor
 Mechanical Factor
 Mechanics of Parturition
 Summery
 References

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Introduction
Parturition is the biological activity in which the fully mature baby is
expelled out from the uterus of the mother's body after the end of the gestation
period. It requires the presence of regular painful uterine contractions, which
increase in frequency, intensity and duration leading to progressive cervical
effacement and dilatation. In normal labour, there appears to be a time-dependent
relationship between these elements: The biochemical connective tissue changes
in the cervix usually precede uterine contractions that, in turn, lead to cervical
dilatation. All of these events culminate in spontaneous rupture of the fetal
membranes. The mean duration of human singleton pregnancy is 280 days (40
weeks) from the first day of the last normal menstrual period. “Term” is defined
as the period from 37.0 to 42.0 weeks of gestation. after the last menstruation
period of the mother. For the process of parturition, it is important for the baby to
get mature which in turn secrets or releases some signals hormones for the
expelling out of the baby. After release, this hormone will diffuse into the
mother's blood where they cause secretion of the important hormone Oxytocin.
Oxytocin stimulates the secretion of the Prostaglandin hormone which
simultaneously causes the uterus to contract so that the baby can be easily
expelled out and cause birth.Preterm birth (defined as delivery before 37 weeks'
gestation) and post-term pregnancy (defined as pregnancy continuing beyond 42
weeks) is both associated with a significant increase in perinatal morbidity and
mortality.
Studies in animals have underlined the importance of fetus in control of timing
of labor. Activated fetal hypothalamic-pituitary-adrenal (HPA) axis leads to a
surge in adrenal cortisol production. Fetal cortisol stimulates activity of placental
17 α hydroxylase/17, 20 lyase (CYP 17) enzyme, which catalyzes the conversion
of pregnenolone to estradiol. The altered ratio of progesterone: estrogen in favor
of later, up regulates the synthesis of uterine prostaglandins (PG) and labour.
Human placenta lacks CYP 17 and as such, the mechanism of labour is different.
Parturition in most animals results from changes in circulating hormone levels in
the maternal and fetal circulations at the end of pregnancy (endocrine events),
whereas labour in humans results from a complex dynamic biochemical dialog
that exists between the fetoplacental unit and the mother (paracrine and autocrine
events).

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Initiation of Parturition
Despite decades of research, the events leading to the initiation of labor in humans
remain unclear. It is suspected that biochemical substances produced by the fetus
induce labour. In addition, the timing of the production of these substances and
their interaction with placental and maternal biochemical factors appear to
influence this process. Among the most studied of these biochemical substances
are fetal hormones such as oxytocin and placental inflammatory molecules.
Increased placental and maternal production of inflammatory molecules in late
pregnancy has been strongly linked to the initiation of labour. Hormonelike
substances called prostaglandins, which are produced by the placenta in response
to various biochemical signals, can induce inflammation and are present in
increased levels during labour. Several factors that increase the production of
prostaglandins include oxytocin, which stimulates the force and frequency of
uterine contractions, and a fetal lung protein called surfactant protein A (SP-A).
Surfactant production in the fetal lung does not begin until the last stages of
gestation, when the fetus prepares for air breathing; this transition may act as an
important labour switch.
Signs and Changes During Parturition
Some of the signs and changes that occur during Parturition are as follows:
1. Mucous discharge
2. Bloated abdomen
3. Feeling relentlessness
4. Change in the hormonal levels of the body
5. Labour and Contractions of the myometrium of the uterus
6. Fully swollen vulva
7. Relaxed pelvic ligaments
8. Lactation.

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Hormonal Factor
1. Increase in Estrogen progesterone Ratio
Estrogen
Pregnancy is a hyperestrogenic state. The placenta is the primary
source of estrogen and concentration of estrogen increases with
progressing gestational age. The human placenta lacks CYP 17, needed for
conversion from progesterone to estradiol. The fetal zone of the adrenal
gland produces DHEAS, which may be hydroxylated to 16-OH-DHEAS
in the fetal liver. The 16-OH-DHEAS may be aromatized by the placenta
to produce estriol, the major circulating estrogen of human pregnancy. In
contrast to the nonpregnant state, during late human pregnancy the ovary
is a minor source of circulating estrogens. Estradiol and estrone are
synthesized primarily (90%) by aromatization of maternal C 19 androgens
(testosterone and androstenedione), whereas estriol is derived exclusively
from the fetal C19 estrogen precursor (DHEAS). Estriol concentrations in
serum and saliva increase during the last four to six weeks of pregnancy.
Estrogens promote a series of myometrial changes including
increased production of PG E2 and PG F2α with augmented expression of
PG receptors, increased receptor expression of oxytocin, α adrenergic
agonist which modulate membrane calcium channels, increased synthesis
of connexin and gap junction formation in myometrium, up regulation of

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enzyme responsible for muscle contraction like myosin light chain kinase,
calmodulin. All these changes allow coordinated uterine contractions.
Cervical ripening may be associated with the down-regulation of
the estrogen receptor. The control of the softening of the cervix, which
involves rearrangement and realignment of collagen, elastin, and
glycosaminoglycans such as decorin, is not well studied and is poorly
understood.
Progesterone
Corpus luteum is the source of progesterone till seven weeks of
pregnancy. Placenta takes over the function at approximately seven to nine
weeks of gestation. In pregnancy progesterone is in dynamic balance with
estrogen in the control of uterine activity. Animals demonstrate systemic
progesterone withdrawal as an essential component in initiation of labour.
Humans though do not show fall in circulating progesterone, there is
growing number of evidence that, spontaneous onset of labour is preceded
by a physiologic withdrawal of progesterone activity at the level of uterine
receptors.
Progesterone in vitro decreases myometrial contractility and
inhibits myometrial gap junction formation. Progesterone activity
stimulates the uterine NO synthetase, which is a major factor in uterine
quiescence. Progesterone down-regulates prostaglandin production, as
well as the development of calcium channels and oxytocin receptors both
involved in myometrial contraction. Calcium is necessary for the activation
of smooth muscle contraction. In the cervix, progesterone increases tissue
inhibitor of matrix metalloproteinase 1 (TIMP-1). TIMP-1 inhibits
collagenolysis. Thus, it is clear that progesterone is a major factor in uterine
quiescence and cervical integrity. The factors that result in parturition must
overcome the progesterone effect that predominates during the early
pregnancy period of uterine quiescence. The activity of 17, 20
hydroxysteroid dehydrogenase in fetal membranes increases around the
time of parturition, leading to an increase in net 17β-estradiol and 20-
dihydroprogesterone. This is a factor in altering the estrogen/progesterone
balance. There may be decreased progesterone receptor levels at term
resulting in a diminished progesterone effect.
Cortisol and progesterone appear to have antagonistic actions
within the fetoplacental unit. For example, cortisol increases prostaglandin

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production by the placental and fetal membranes by up-regulating
cyclooxygenase-2 (amnion and chorion) and down-regulating 15-
hydroxyprostaglandin dehydrogenase (15-OH-PGDH) (chorionic
trophoblast), thereby promoting cervical ripening and uterine contractions.
Progesterone has the opposite effect. In addition, cortisol has been shown
to compete with the inhibitory action of progesterone in the regulation of
placental CRH gene expression in primary cultures of human placenta. It
is likely, therefore, that the cortisol-dominant environment of the
fetoplacental unit just before the onset of labour may act through a series
of autocrine-paracrine pathways to overcome the efforts of progesterone to
maintain uterine quiescence and prevent myometrial contractions.
 Progesterone – decrease excitability and contractility
 Estrogen – increase excitability and contractility
 During the early 30 weeks of pregnancy estrogen to progesterone ratio is
balanced
 After about 30th week
- estrogen continue to increase
- progesterone reaches a stationary level
- E/P is increased
- contractility progressively increases
- labour begins when progesterone’s inhibition is overcome by an
increase in the level of estrogen
Release of Oxytocin
Circulating oxytocin does not increase in labour until after full
cervical dilatation.Oxytocin is less effective in causing uterine contractions
in mid pregnancy than at term. However, the concentration of uterine
oxytocin receptors increases toward the end of pregnancy. This results in
increased efficiency of oxytocin action as pregnancy progresses. Estrogen
increases oxytocin receptor expression and progesterone suppresses such
estrogen-induced increase in cultured human myometrial cells. Oxytocin
induces uterine contractions in two ways. Oxytocin stimulates the release
of PGE2 and prostaglandin F2α in fetal membranes by activation of
phospholipase C. The prostaglandins stimulate uterine contractility.
Oxytocin can also directly induce myometrial contractions through
phospholipase C (PLC), which in turn activates calcium channels and the

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release of calcium from intracellular stores. Oxytocin is locally produced
in the uterus. The role of this local endogenous oxytocin is unknown.
- oxytocin has been proved to be involved in increased contraction of
the uterus
* oxytocin receptor in uterine muscles increase in the later part of
the Pregnancy
* Rate of oxytocin secretion has been seen to be high at the time of
delivery
* Absence of posterior pituitary – prolonged labour
* Experimental irritation or stretching of the cervix increases the
production of oxytocin

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2. Foetal Hormone
- Fetal posterior pituitary produce large amount of oxytocin
- foetal adrenal cortical cortisol is also oxytocic
- Prostaglandins from the fetal membrane towards the end of
pregnancy help the contractility during labour
Corticotropin-releasing Hormone (CRH)
i. Corticotropin-releasing hormone (CRH) is released by the placenta during
pregnancy, which in nonpregnant women is secreted only by neurosecretory cells
of the hypothalamus.
ii. CRH acts as the “clock” that establishes the timing of birth.
iii. High levels of CRH during the early stages of pregnancy in a woman can
result in premature pregnancy delivery, whereas those who have low levels are
more likely to deliver after their due date.
iv. CRH regulates the timing of birth by altering the signalling pathways and
systems that are responsible for controlling the contractile properties of the
smooth muscles of the myometrium of the uterus.
v. Secretion of CRH by the placenta increases enormously, usually 1000−10000
times more than a normal and nonpregnant woman.
Prostaglandins
Prostaglandins are formed from arachidonic acid that is converted to
prostaglandin H2 by the enzyme prostaglandin H synthetase (PGHS). PGHS-2 is
an inducible form of the enzyme. Cytokines increase the concentration of this
enzyme 80-fold. Prostaglandins are degraded by 15-OH-PGDH. Cyclo-
oxygenase-2 (COX-2) is cytokine inducible, is increased by NO. This is another
mechanism by which prostaglandin production increases during inflammation.

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There is good evidence that prostaglandins are involved in the final
pathway of uterine contractility and parturition. Prostacyclins, inhibitory
prostaglandins present throughout early pregnancy, are also responsible for
uterine quiescence during pregnancy. Although prostaglandins may not be
obligatory for labour in knockout mice, they are of major importance in women.
Prostaglandins are produced in the placenta and fetal membranes. Prostaglandin
levels are increased before and during labour in the uterus and membranes.
PGF2α is produced primarily by the maternal decidua and acts on the
myometrium to up-regulate oxytocin receptors and gap junctions, thereby
promoting uterine contractions. PGE2 is primarily of fetoplacental origin and is
likely more important in promoting cervical ripening (maturation) associated with
collagen degradation and dilation of cervical small blood vessels[ and
spontaneous rupture of the fetal membranes. Many factors affect the production
of prostaglandins. Levels are decreased by progesterone and increased by
estrogens.Several interleukins result in an increase in prostaglandin production.
Relaxin
Relaxin is a peptide hormone that is a member of the insulin family.
Relaxin consists ofAand B peptide chains linked together by two disulfide bonds.
In women, circulating relaxin is a product of the corpus luteum of pregnancy.
Circulating relaxin is secreted in a pattern similar to that of human chorionic
gonadotropin. That circulating relaxin is not critical for pregnancy maintenance
However; relaxin is also a product of the placenta and decidua. Relaxin from these
sources, which may act locally, is not secreted into the peripheral circulation.
Relaxin receptors are present on the human cervix. Some of the effects of relaxin
include stimulation of procollagenase and prostromelysin, as well as a decrease
in TIMP-1. Relaxin is also capable of inhibiting contractions of non-pregnant
human myometrial strips. Paradoxically, relaxin does not inhibit contractions of
pregnant human uterine tissue. This may be because of the competitive effects of
progesterone.

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Mechanical Factor
1. Onset of labour
 This is the forceful muscular contraction of the uterus that happens at the
time of birth. As this process requires some sort of energy along with the
work that’s why this process is given the name Labour.
 When the mother reaches the end of the gestation period the baby turns its
position in which the head portion remains in downward and the leg portion
remains upwards.
 The labour starts after the completion of the gestation period which causes
labour pain.

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Mechanics of Parturition
Stages of Parturition
There are three Stages of Parturition
1. Dilation
Dilation is defined as the uterus beginning to enlarge and rupture the
membranes. It also starts a bloody discharge progressively. Dilation is
usually the first stage of the process of labor. It starts when the effaced
cervix is 3 cm dilated. Though it varies across women and they might not
even have been experiencing active contractions before reaching this stage.
During this process, the cervix becomes combined into the lower segment
of the uterus. Parturition shortens the mussels and upper segments. It is
drawing upwards and the lower segment during a contraction, and gradual
expulsive motion upwards.
When the cervix has enlarged, the presenting fetal part permits to descend
enough to allow passage for the baby’s head. It is around 10 cm for a full-
term baby, here the process of dilation is complete. The actual period of
the labor process varies slightly, though the average duration for the active
phase is around 20 hours.
During the active phase, the cervix will dilate at a rate of about 1 cm/hr for
a woman who’s giving birth for the first time. For a woman who’s
previously had a vaginal delivery, the rate is typically about 2 cm/hr. This
concept has been explained with the help of Friedman’s Curve, which
focuses on the standard rate of fetal descent and cervical dilation during
active labor.

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This stage is divided into a latent phase, an active phase and a transition
phase.
a. Latent Phase
i. This phase lasts about 6 to 12 hours.
ii. The latent phase or early labour phase begins with mild, irregular uterine
contractions that soften and shorten the cervix.
iii. As contractions begin, the walls of the uterus start to contract through
stimulation by the release of the hormone oxytocin secreted from the
posterior pituitary.
iv. The contractions cause the cervix to widen and begin to open.
v. It results in the discharge of fluid and a bit of abdominal discomfort.
vi. The water may break, i.e., rupture of the amniotic sac membrane or
amnion takes place, and it flows out through the vagina.
b. Active Phase
i. The active phase of the dilation stage generally lasts up to 3 to 6 hours.
ii. This phase begins when the cervix is about 3–4cm dilated.
iii. The active phase is characterized by further dilation of the cervix and
descent of the fetal part towards the cervix.
iv. Contractions become progressively more rhythmic and stronger.
c. Transition Phase
i. It lasts for 20 to 30 minutes and contractions are initiated at an interval
of about every 1 to 3 minutes.
ii. The contraction of the myometrium is very intense.
iii. Cervix dilates from 7 up to 10cm
i.e., complete dilation

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2. Expulsion
This second stage of parturition starts at full dilation and continues
until birth. This parturition process commences when the cervix pressure
of the uterus increases, and in turn, the uterus Ferguson reflex increases
uterine contractions. At the start, the top portion is completely engaged
within the pelvis, i.e., the widest diameter of the pinnacle has passed below
the amount of the pelvic inlet. Thereafter, the head of the baby continues
descending into the pelvis, then below the pubic arch, and finally out of the
vagina.
The fetal head is assisted by extra maternal efforts or pushing down. The
successful birth of the marks the completion of the second stage of
parturition. Important factors, such as parity, fetal size, anesthesia, will
cause variations in the second stage of delivery.
3. Placental Birth
This third stage of parturition starts after birth and ends with the
delivery of the placenta. The normal duration between the delivery of the
baby and the placenta varies between 10–12 minutes. It is often managed
by giving a uterotonic, like oxytocin, together with appropriate cord
traction. A fundal massage that is administered by a qualified birth
attendant assists in delivering the placenta. Alternatively, it is allowing the
placenta to be expelled without medical assistance.
The infant is more often than not born with the membranes still intact when
the amnios have not ruptured during labor or pushing. It is often mentioned
as being taken within the caul. It does not cause any harm, and moreover,
the membranes can be easily wiped and broken away.
4. Labor
This is the forceful muscular contraction of the uterus that happens at
the time of birth. As this process require some sort of energy along with the
work that's why this process is given the name Labour. When a mother
reaches the end of the gestation period the baby turns its position in which
the head portion remains in downward and the legs portion remains
upwards. The labour starts after the completion of the gestation period
which causes Labour pain in the body.

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Summary
parturition, or birth or childbirth or labor or delivery, the process of bringing forth
a child from the uterus, ending the pregnancy. It has three stages. In dilation,
uterine contractions lasting about 40 seconds begin 20–30 minutes apart and
progress to severe labor pains about every 3 minutes. The opening of the cervix
widens as contractions push the fetus. Dilation averages 13–14 hours in first-time
mothers, less if a woman has had previous babies. When the cervix dilates fully,
expulsion begins. The “water” (amniotic sac) breaks (if it has not already), and
the woman may actively push. Expulsion lasts 1–2 hours or less. Normally, the
baby’s head emerges first; other positions make birth more difficult and risky. In
the third stage, the placenta is expelled, usually within 15 minutes. Within six to
eight weeks, the mother’s reproductive system returns to nearly the pre-
pregnancy state

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References
 “Medical Physiology” Elsevier (2016)
 “Physiology” Elsevier (2017)
 “Human Anatomy and Physiology” Pearson (2018)
 “Principle of Anatomy and Physiology” Wiley (2014)
 “Reassessing the labor duration in nulliparous women” American Journal
of Obstetrics and Gynaecology (2015)

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