Mammalian Birth
Changes required at birth
Requirement for specific and fully organised neurological/reflex pathways
Hormonal function (cf steroids – most peptide hormones cant cross the placenta)
Epidermal function (barriers)
Loss of placenta impacts on:
Heat generation (Changes from requiring to loose – to needing to maintain)
Intestinal function (increases and becomes critical for life) – movement (including
suckling) – digestion – absorption
Liver function (increases and becomes critical for life)
Renal function (excretion and increased resorption of ions/glucose and becomes
critical for life)
Lung function (starts and becomes critical for life)
Cardiovascular changes (driven by need for above)
Roles of the placentra
Transfer of gases – O2/CO2
Transfer of nutrients – Glucose, AA, triglycerides – transporters (NB no transfer of
triglyceride directly – triglycerides absorbed and lipase in fetal placental cells
releases FAs)
Transfer of urea and NH3 (latter sent to maternal liver/kidney), uric acid, creatinine
Heat transfer sink
Transfer of IgG to foetus (specific) – transfer across the syncytiotrrophoblasts of the
chronic villi mediated by the neonatal Fc receptor, FcRn and endocytosis
Circulatory reservoir
Immune modulator of foetus – active suppression of host-vs-graft eraction
Hormone production – chorionic gonadotropin (maintains the corpus luteum) –
progesterones – CRH/oestrogens – Placental lactogen (increases maternal serum
glucose) – prostaglandins (nb normally auto or paracrine)
Placenta issues
1. before birth we must retain the umbilical vessel patent
2. At birth we must transfer blood to the foetus from the placenta
3. We must then close the placental circulation
Approx. 33% of all neonates placental blood volume is in the placenta – its loss
would be dangerous for the baby
Approx. 30% transfuses in the first 15 seconds after birth
Approx. 60% transfuses over following the 2-3 minutes
Caused by the positional differences and contractions of the uterus to express the
placenta immediately after birth create a pressure gradient between the placenta
and the neonate
, Umbilical vessels
Umbilical arteries do not possess an internal elastic membrane and contain little
elastin, in general, while the vein contains an elastic layer but no valves
The arteries also lack the adventitia seen in cardiovascular vessel – instead, rigid
Wharton’s jelly performs the function of the adventitia
Wharton’s jelly is a gel-like porous ECM – the fibrous scaffold is made of collagen and
elastin – the pours contain proteoglycans, (mainly versican) and hyaluronic acid that
bind water to form a viscous fluid – this is held by an outer epithelial layer
continuous with the amniotic epithelium
The jelly contributes to the firmness of the intact cord
Two umbilical arteries coil around the vein in a helical fashion
Blood flows in a pulsatile manner from the foetus to placenta through the arteries
A small pulse remains in the more passive transfer of blood back to the foetus
through the umbilical vein
Umbilical coiling appears to confer turgor to the umbilical unit – producing a cord
that is strong but flexible – low umbilical coiling index is an indicator of adverse
perinatal outcome
Wharton’s jelly surrounding the foetal vessels can withstand torsional and
compressional forces
Occasionally, Wharton’s jelly does not develop in all portions of the cord – at this
point the foetal vessels are no longer protected from torsional closure
The lining endothelial cells of the umbilical vessels are highly metabolically active
and form two major dilatory factors PGE2 (other vessels esp heart endothelia form
PGI2) and NO
Before birth patent/relaxed umbilical circulation
Maintained through gestation
No nervous input to placental vasculature
Little effect of catecholamines
The contractility of smooth muscles in vessel walls is influenced by paracrine signals
produced by the neighbouring endothelial cells
PGE2 and NO
NO – expression driven by shear flow and endothelin, Bradkinin and atrial natriuretic
peptide – all-cause vasodilation s umbilical arteries relaxed and patent
At birth umbilical circulation closes
40-60s – reduction of blood flow by 80%
1. Reduction of PGE2 synthase in vessels – umbilical arteries earlier than vein
2. Local mediators (induces constriction lasting 2-3hrs) – increased local thromboxane –
increased serotonin
3. Stretching of umbilical cord can cause spasm
4. Cooling to 18oC (short term 10-20 mins effect)
5. High external oxygen tensions (closes the artery, not the vein)
All leads to clamping of the vessels – functionally closed within 2-3mins of birth
Placental vessels summary
Retained open during pregnancy
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