2 – Prolonged partial asphyxia
In Myers' (1972) experiments, prolonged partial
asphyxia was produced before birth, in most cases by
mechanical constriction of the materal abdominal
aorta (distal to the renal arteries). Other
manipulations included: (a) partial placental ablation,
(b) catecholamine infusions into the maternal
circulation to produce maternal visceral
vasoconstriction, (c) use of fluorothane to produce
maternal hypotension, and near-term (d) infusion of
excessive oxytocin into the maternal bloodstream,
which stimulated frequent strong uterine contraction.
All of these methods reduced maternal blood flow
and perfusion of the placenta [1].
Fetal heart-rate, blood pressure, blood oxygen, and
degree of acidosis were monitored and correlated
with three identifiable postnatal outcomes:
- Mild asphyxia with pH levels maintained above
7.10 and fetal blood oxygen above 1.5 to 2.0
volumes percent resulted in no evidence for
brain injury on either clinical or pathological
examination.
- Severe asphyxia with pH below 7.00 and fetal
blood oxygen below 0.4 to 0.8 percent
enduring for several hours leads to fetal death
from heart failure. Even if resuscitated and
maintained in intensive care for many hours,
the newborn monkeys were unable to maintain
normal blood pressure and died due to
progression of hypotension. Brain pathology
was difficult to evaluate because of their short
survival, but brain swelling and necrosis in the
cerebral hemispheres was noted.
- Intermediate degrees of asphyxia permitted
survival but with evidence of permanent injury
of the brain and heart. "Asphyxial myocardial
decompensation" was identified as a factor in
impaired postnatal circulation and consequent
diminished perfusion of the brain. Swelling of
the brain was discussed as a further
compounding factor, "Severe brain swelling
expressed the blood from the cerebral
vasculature, leaving the entire brain pale and
bloodless" [1, p265].
- Myers RE (1972) Two
patterns of perinatal brain
damage and their
conditions of occurrence.
Reference